Research Question of the Week: How to Optimize Fat Efficiency in the Diet

[Venom]

Introduction

Fat is often given a bad rap. However, it has many vital purposes. These include (Inouye, 2005):

1. Phospholipid structure
2. Cell membrane structure
3. Storage of fat soluble vitamins
4. Production of hormones
5. Storage form of energy (adipose tissue)
6. Supply of energy through beta oxidation.

The goal with fat for a bodybuilder is to optimize the nutrient partitioning effect. Nutrient Partitioning can be defined as the distribution of ingested nutrients among basal metabolism, growth, tissue maintenance and repair, physical activity, and other forms of energy expenditure and nutrient storage. The goal is to partition nutrients away from fat storage, and towards these other vital functions that fats have, such as increased hormones.

Consuming the correct proportion of certain fats can help accomplish just this. Before proceeding, the various types of fats that exist must be opperationaly defined.

Saturated fats have a full quota of hydrogen’s and are therefore, very stable. Rich sources of these fats include butter, animal products, and coconut oil.

http://www.abcbodybuilding.com/saturated.jpg

Figure 1.

A diagram of a saturated fatty acid. The “OH” is the acid tale, or hydroxyl group.

Unsaturated fatty acids have double bonds and therefore, less hydrogen’s. Two classifications of unsaturated fats are: monounsaturated and polyunsaturated fats. Monounsaturated fats have one double bond, and are therefore, much more reactive (less stable). Rich sources of these fats include grape seed oil, olive oil, canola, peanut oil and avocado.

http://www.abcbodybuilding.com/monunsaturated%20fat.jpg

Figure 2.

Figure two is a diagram of a monunsaturated fatty acid. Notice it contains only one double bond on the carbon atoms.

Polyunsaturated fats contain 2 or more double bonds. Rich sources of these fats include safflower, flax, fish, and walnuts.

http://www.abcbodybuilding.com/essential_fatty_acids_files/hch2.gif


Figure 3.

Figure 3 depicts the polyunsaturated fatty acid, Alpha-linolenic Acid.

The length of a chain of carbons also determines the classification of the fatty acid.

>8 are short chain fatty acids
8-12 carbons are medium chain
16 + = long chain fatty acids

Evidence suggests that short and medium chain fatty acids can actually diffuse into mitochondria without carnitine transferase, which is important for their ability to be oxidized. This is why medium chain FFA's are often used for say malabsorbtion sydromes of fats.

There are three main differences between long and medium chain fats:

1. Chain length
2. Solubility - medium chains are more soluble in water
3. Medium chains can diffuse into the mitochondria without carnitine transferase

In this context, medium chains TG's are actually preferentially oxidized.

One of the ways to measure if a food is being used for energy or not is to measure oxygen consumption before and after the nutrient is taken in.

In one study (Brody, 2003) people consumed 45 grams of long or medium chain fatty acids. Oxygen was measured to determine energy used. 02 consumption increased slightly in the long chain condition, but a larger increase occurred in medium chain condition. This is consistent with long chain FFA's being first stored as fat, with medium chain ffas being oxidized instead. In 6 hours following test meals, 13 % of medium chain and 4 % of long chain were completely oxidized. Thus, fat oxidation is relative to the fat substrate.

Therefore, medium chain FFA's are less likely to be stored as fat, and more likely than long chain FFA's to be used as fuel. However, this depends on the type of long chain triglyceride. For instance, essential fats are long chained fatty acids; but, they have been found to increase insulin sensitivity, thermogenesis, anabolic hormones, anti-inflammatory cytokines, among numerous other benefits (Wilson, G. 2003).

For more information on essential fatty acids, refer to Wilson, G (2003) Essential Fatty Acids - An In Depth Analysis.

It has been shown that fat plays a key role in the formation of anabolic hormones.

Goldin et al. (1994) investigated the effect of dietary fiber and fat on serum sex hormones in premenopausal women. Participants consisted of 48 women, who’s diets were high in fat (40% of calories as fat) and low in fiber (12 g/day). Participants then changed to a low-fat (20-25% calories as fat) and high fiber (40 g/day) diet. Results found that there were significant decreases in serum concentrations of estrone, estrone sulfate, testosterone, androstenedione, and sex hormone binding globulin (SHBG) and near significant decreases in estradiol and free estradiol.

Hamalainen et al. (1994) had participants decrease fat from 40-25% and found a decrease in the serum concentrations of androstenedione, testosterone and free testosterone.

Ingram (1987) randomly assigned thirty-three women in good health to commence either a standard diet (deriving 40% of their energy from fat) or a low-fat diet (deriving 20% of their energy from fat), for two months, in a cross over study, which lasted a total of 16 weeks. Low-fat diets appeared to decrease levels of both non-protein-bound estradiol (1.48 down to 1.27%; P = .07) and non-protein-bound testosterone (1.06 down to 0.86%; P = .11). Cholesterol levels were lowered by the low-fat diet and were significantly associated with estradiol, testosterone, and dehydroepiandrosterone.

In a related study, Reed et al. (1987) found similar results. He also found that Changing the diet from one with a high fat to low fat content (less than 20 g fat/day) for a further two week period resulted in a significant reduction in mean plasma cholesterol levels (p less than 0.001); while the mean SHBG levels increased (p less than 0.01).

Volek et al. (1997) found that subjects eating a moderate fat diet exhibited higher testosterone levels than subjects eating low-fat diet. Additionally, they found that monounsaturated and saturated fat raise testosterone levels, but polyunsaturated fat do not.

As discussed, Reed et al. (1987) found that Changing the diet from one with a high fat to low fat content (less than 20 g fat/day) for a further two week period resulted in a significant reduction in mean plasma cholesterol level (p less than 0.001) while the mean SHBG level increased (p less than 0.01). Thus, another action of fat is to decrease levels of SHBG.

Concerning SHBG, this binds testosterone, temporarily constraining steroid hormones from exerting their activities. Therefore, by lowering levels of SHBG, you will raise the amount of free steroid hormones in the body.

While saturated fats clearly are beneficial for raising anabolic hormones, evidence suggests they have several deleterious effects. Here is a quote from Wilson, G. (2003) explaining one of these effects:

[ QUOTE ]
Insulin Sensitivity

If you have read any of our articles, you know just how valuable insulin sensitivity is. Simply put, increased sensitivity promotes a much greater anabolic response to insulin and increases your fat-burning ability immensely, while insulin resistance leads to elevated fat storage, reduced hypertrophy, and increased susceptibility to diseases such as diabetes. For more, study the following articles: Metabolic Primer Part I, and Endocrine Insanity Part III.

Here is the exciting part: studies show omega-3s can increase insulin sensitivity drastically, while its counterpart--omega-6s--in higher dosages may lead to insulin resistance.

For instance, a fascinating study was performed on rats using high-fat diets and various lipids to assess their effect on bodyweight regulation, adiposity, and metabolism. Results showed that rats who consumed high amounts of saturated or n-6 polyunsaturated fatty acids became obese, insulin resistant, and gained the most fat, while fish oils showed to be a superior fat in the experiment [57].

Another study stated that the negative effects of a high-sucrose diet, which induced insulin resistance and mild glucose intolerance, were counteracted by enhanced dietary intake of omega-3 polyunsaturated fatty acids [51].

Storlien LH et al. tested the effects of certain fats on rats. Subjects who had diets rich in polyunsaturated (omega-6) fatty acids developed severe insulin resistance. Afterward, they substituted 11% of the fatty acids in the polyunsaturated fat diet with long-chain omega-3 fatty acids from fish oils. The omega-3s were shown to effectively normalize insulin action [66].

Furthermore, Chicco A et al. composed a diet with 7% of the calories coming from cod liver oil--which is rich in omega-3 fatty acids--on male Wistar rats. The end results showed a significant reduction in plasma insulin levels throughout the day, due to enhanced insulin sensitivity [11].

Popp-Snijders C et al. performed an excellent study for the effects of Omega-3s on diabetics. Six non-insulin-dependent diabetics supplemented with just 3 g of the omega-3 fatty acids daily, over an 8 week time span. The subjects showed enhanced insulin sensitivity and lower plasma triglyceride levels [55].

Another experiment was performed on rats. First, they implemented a diet high in omega-6 and saturated fatty acid, which again lead to insulin resistance. Afterward, they replaced simply 6 percent of the linoleic omega-6 fatty acids from safflower oil with long-chain polyunsaturated omega-3 fatty acids from fish oil. This resulted in the prevention of insulin resistance [62].

It should be noted that in Western society diabetes has become a prevalent disease. This can be largely attributed to the lopsided ratio of omega-6:3 fatty acids. Diabetics will want to take close notice of these results, and adjust their diets accordingly [62].

So, as you see, a diet rich in Omega-6s can lead to insulin resistance, while a diet full of Omega-3s will inevitably increase insulin sensitivity [39,40,14].

[/ QUOTE ]

In summary, a high dosage of omega 6 or saturated fatty acids increases insulin resistance and fat gain. While omega 3 fatty acids have been shown to enhance insulin sensitivity and fat oxidation.

A high fat diet has also been shown to decrease satiety. Here is another quote from Wilson, G. (2003) in his article on satiety explaining:

[ QUOTE ]
Studies show that humans adapt very quickly to high fat diets (HFD), which subsequently decreases the satiating response to nutrients. For instance, Cunningham et al. showed that consumption of a high-fat diet for two weeks led to an acceleration in the gastric emptying rate of high-fat test meals [59]. However, CCK is still raised very high during HFD, making these results rather strange [60]. To test the mechanisms by which this adaptation occurs, Covasa and Ritter injected CCK into rats on low fat diets and high fat diets [61]. The former group had a much slower rate of gastric emptying (26.2-55.1%) than the later group (10.0-31.7%). This shows that HFD may cause subjects to be insensitive to CCK’s satiating effects.

To further investigate this, French et al. had 12 male subjects consume a high-fat diet (58% energy) for two weeks, testing levels of cholecystokinin (CCK), food intake, and subjective feelings of hunger and fullness [62]. The results showed a significant enlargement in the average daily food consumption, increasing feelings of hunger and declining fullness. And again, CCK was substantially higher, further supporting the hypothesis that high-fat diets reduce the body’s sensitivity to this hormone.

Castiglione, Read, and French sought to test whether this effect on gastric emptying was nutrient-specific [63]. Studies were carried out on eight healthy, free-living male volunteers between the ages of 19 and 26. Their original fat intake was between 30-40%. In the test they increased this to 55% for 14 days. They then gave them high-fat and high-carbohydrate meals. The high carbohydrate meals had nearly the same rate of gastric emptying before and after the experiment. However, the rate of lipid emptying was much faster, consistent with the previous experiments. This shows HFD adaptations are nutrient-specific to fats, and not to carbohydrates.

Now, most athletes never would have this much fat in their diet. However, this does show the folly in excessively high-fat/low-carb diets, which not surprisingly often advocate the wholly ignorant, logically invalid, and completely unscientific protocol of fat and fiber post-workout. Moreover, you can see that people who eat junk food constantly (i.e. pizza) are going to be much more susceptible to continued binges than someone on a lower fat diet. To exemplify the harm in this adaptation, rats fed the same amount of fat at a slow rate consumed less energy per day, had longer between-meal intervals, and gained less weight over a two-week period than after infusion of fat at a more rapid rate [125]. So, those reading need to take a close look at their diet, and be sure they are not consuming excessive amounts of fat right now.



[/ QUOTE ]

Fat efficiency is therefore, of the utmost importance, as consuming to much fat is unhealthy, will promote fat storage, lower satiety, among numerous other negative effects.

While the polyunsaturated fats Alpha-Linolenic Acid and Linoleic Acid have been thoroughly investigated by Wilson, G. (2003) questions still remain on the consumption of various other fats, especially when considering that polyunsaturated fatty acids are ineffective in raising testosterone levels.

Bodybuilders are often proponents of large consumptions of meats such as steak which are rich in saturated fatty acids. As displayed, this would elicit anabolic benefits such as increased testosterone, but it also will have deleterious effects such as lowered insulin sensitivity.

However, while medium chain triglycerides are a type of saturated fat, studies have found that they are excellent for increasing fat oxidation, contrary to reports on supplementation with other saturated fatty acids. If these fats therefore elicited the same anabolic benefits as other saturated fatty acids, they would be of practical importance to the athlete.

In this context, the purpose of this thread is to discuss how to optimize fat efficiency in the diet. Of particularly interest is the effect of medium chain triglycerides on hormones such as testosterone. Posts on the benefits of any type of fat, scientific studies to support claims, and theoretical rationales behind these claims are promoted.

[l0stsheep]

WOW...great article here Venom!

I wish I had something to add to the thread, but since I do not, I will just soak up the information! /forum/images/graemlins/smile.gif

[President Wilson]

One thing I want to mention is that these questions of the week are big issues in our field.

We are very serious about this subject and would like to do some experimental research on it. So any research you guys have or studies are awesome. We'd love to hear your insight!

[Venom]

Yup, if you guys come up with a convincing argument, or propose some research, we could try to do a study! /forum/images/graemlins/laugh.gif

[stillflabby]

My comment doesn't really add anything here, but I just want to say I am continually impressed with this site. The level of information here and the knowledge the maintainers possess is truely impressive.

You all are an inspiration and makes me want to get back into the medical field.

[Venom]

Oh wow! That is fantastic, bro. Thank you for sharing your testimony. /forum/images/graemlins/grin.gif

[Bahir]

I dont have anything to add either, but I just want to say that this whole thing is a fantastic idea. Great work!

[Venom]

Thanks, guys!

Also, please don't feel that you guys have to post a long scientific explaination. It would be fantastic if anyone wanted to suggest theories on this or propose their own questions on other things that can be researched. Personal experiences are also more than welcome. /forum/images/graemlins/smile.gif

[book]

[ QUOTE ]
Thanks, guys!

Also, please don't feel that you guys have to post a long scientific explaination. It would be fantastic if anyone wanted to suggest theories on this or propose their own questions on other things that can be researched. Personal experiences are also more than welcome. /forum/images/graemlins/smile.gif

[/ QUOTE ]

Question: What ratio of fats would be best on a cut?

[Qester]

If one were to take a minimal fat diet would it counter-act any intake of longer lipids, since the decrease would lower the amount of cholesterol which would result in a lower amount of cholesterol in the lipid bi-layer allowing for more flexibility and thus allowing it to become more permeable? Resulting in a higher oxidization in the long run, And through these long side chain lipids you would therefore increase the amount of anabolic hormoes?

[Venom]

[ QUOTE ]
Question: What ratio of fats would be best on a cut?

[/ QUOTE ]

You mean PCF, or the ratio of mons:polys:saturated.

[ QUOTE ]

If one were to take a minimal fat diet would it counter-act any intake of longer lipids, since the decrease would lower the amount of cholesterol which would result in a lower amount of cholesterol in the lipid bi-layer allowing for more flexibility and thus allowing it to become more permeable? Resulting in a higher oxidization in the long run, And through these long side chain lipids you would therefore increase the amount of anabolic hormoes?

[/ QUOTE ]

It is hard to answer this without knowing what fats are low and what fats are high. So I would need more specifics.

I learned a lot reading the original post, but I'll be honest. .... I am clueless and have nothing to add!
/forum/images/graemlins/smile.gif

[Endless]

I know this won't really help because research stuff is not my strong point, but I was looking at articles trying to find some info about this and I found one article that seems to be relevant, but I can't find the full-text version. I know, it's stupid of me to judge based on the abstract alone, but it's all I've got right now. Perhaps you have some magical research article powers and you can find the full text...if not, I'll keep looking. Anyway, here's what the abstract says:

"There is considerable epidemiological evidence that a Western-style diet may increase the risk of certain hormone-dependent conditions in men via its effects on hormone metabolism. Experimental evidence also suggests that dietary factors may exert subtle effects on hormone metabolism. Here we review the clinical and epidemiological evidence that diet is associated with circulating sex hormone levels in men. In comparison with factors such as age and BMI, nutrients do not appear to be strong determinants of sex hormone levels. Dietary intervention studies have not shown that a change in dietary fat and/or dietary fibre intake is associated with changes in circulating sex hormone concentrations over the short term. The data on the effects of dietary phyto-oestrogens on sex hormone levels in men are too limited for conclusions to be drawn. Observational studies between men from different dietary groups have shown that a vegan diet is associated with small but significant increases in sex-hormone-binding globulin and testosterone concentrations in comparison with meat-eaters. However, these studies have not demonstrated that variations in dietary composition have any long-term important effects on circulating bioavailable sex hormone levels in men. This lack of effect may be partly explained by the body's negative feedback mechanism, which balances out small changes in androgen metabolism in order to maintain a constant level of circulating bioavailable androgens. It appears, therefore, that future studies should look for dietary effects on the feedback mechanism itself, or on the metabolism of androgens within the target tissues."

Article: The effects of diet on circulating sex hormone levels in men
Authors: Allen-NE; Key-TJ
Nutrition-Research-Reviews (NUTR-RES-REV) 2000 Dec; 13(2): 159-84 (159 ref)

Just based on this info, does this agree with what you told me earlier, Venom?
-endless

[book]

[ QUOTE ]
[ QUOTE ]
Question: What ratio of fats would be best on a cut?

[/ QUOTE ]

You mean PCF, or the ratio of mons:polys:saturated.

[ QUOTE ]

If one were to take a minimal fat diet would it counter-act any intake of longer lipids, since the decrease would lower the amount of cholesterol which would result in a lower amount of cholesterol in the lipid bi-layer allowing for more flexibility and thus allowing it to become more permeable? Resulting in a higher oxidization in the long run, And through these long side chain lipids you would therefore increase the amount of anabolic hormoes?

[/ QUOTE ]

It is hard to answer this without knowing what fats are low and what fats are high. So I would need more specifics.

[/ QUOTE ]

Mons:poly:saturated

Though in hind sigh I can see there really wouldn't be much variation now I read up on some things.

[Venom]

Great research endless!!!

That article looks really interesting. I will try to find it in my library.

It definitely is pertinent to this subject, as it discusses the effects of diet—particularly fats—on sex hormones, and also SHBG. That was an interesting comment on negative feedback mechanisms. I have not seen a study that showed an asymptote in increased testosterone and increased fat intake. I.E. would having a diet with 30% saturated fats, produce as much testosterone as a diet with 20% saturated fats? I have only been able to study this indirectly through observation, but I have yet to see a study who’s goal was to examine this question. So that would be a great study. I discussed this with Dr. Brown, and he suggested that ingestion of more fats may not produce more anabolic hormones such as testosterone, as there are to many stages involved. But again, I have yet to see studies which show an asymptote.

[Venom]

Hey, book /forum/images/graemlins/smile.gif

[ QUOTE ]


Mons:poly:saturated

Though in hind sigh I can see there really wouldn't be much variation now I read up on some things.

[/ QUOTE ]

I would say that is a very difficult question, and partially the purpose of this thread. It needs to be investigated!

I will say this: there is no set optimal dosage for either of those fats.

Wilson, G (2003) covered polyunsaturated fats extensively in his EFA article. He suggested that At least 30% of your daily fat should come from EFAs, while using a a 2:1 and 3:1 ratio of omega-3:omega-6. This recommendation was contrary to the mantra that has been spread by numerous others that your omega 6:3 ratio should actually be higher. This was based on clear scientific data suggesting omega 3’s were superior to omega 6’s.

Typically, it is recommended not to have more than 10% of your calories from saturated fats. But this is based on its negative effects. If my research hypothesis is correct, that medium chain triglycerides can elicit the anabolic benefits of saturated fats without these negative effects, that would destroy the entire foundation of this recommendation.

Another issue is that bodybuilders often increase their saturated fats to enhance testosterone production during bulks, and decrease them to avoid fat gain during cuts. But again, studies on MCT may change this mindset.

Monounsaturated fats have been associated with improved cardiovascular health in various studies, so most are strong advocates of its use.

But the optimal ratio is something I have not determined, yet. One of our goals this year in JHR is to discuss Saturated fats, Monounsaturated fats, Polyunsaturated fats, and MCT’s. Within we want to cover their benefits, side effects, and the optimal dosage for each, and if this would vary during cutting and bulking phases. Further, we plan to break down individual fats within these classes (i.e. omega 3 vs. 6 polyunsaturated fats). So stay tuned!

[book]

This is bringing back memories. I remember a REALLY REALLY old post on bulking that reccomended 'Heavy Cream' as a fat source since it was high in MCT's. Now research is actually backing it up /forum/images/graemlins/laugh.gif

[Grimm932]

hi, I have a couple of questions:

1. How much saturated fat should one aim to consume on a daily basis (what % of their total fat calories should come from fat intake)? Is it ok to have foods like heavy cream replace flax oil once in a while because of the benifits offered (increase in anabolic hormones) by saturated fats? and by once in a while i mean: for one protein/fat meal once a week or so. what would be good sources of saturated fat? whole cheese and other dairy products? or meat?

2. Is fresh coconut flesh a good source of MCTs? Are MCTs good to consume while bulking also? should I consume them from food sources or get a supplement that has pure MCT?

Thanks so much for your help and sharing your knowledge.

[stillflabby]

Would eating medium chain TGs actually inhibit to a certain degree your body's ability to burn fat it has stored? Or would it speed this up a bit?
I'm thinking, if your diet contains these fats that are more quickly oxidized, will your body use these up first (not taking into account carb oxidation), then call on fat stores for energy?

I would be interested to see an article that talks about the mechanism fat stores in the body are broken down for energy. At what point do they get tapped into?

I'll try to find an article discussing this, but if someone knows of one, I'd appreciate a heads up.

[Venom]

Hi, Grimm!

To your first question, as I told book, the optimal ratio is something we are still investigating.

But there is no question about this: saturated fats need to be included in your diet if you want optimal results. So yes, if you want to add some that is perfectly fine. Those types you choose would work good.

I know Old School has supplemented with them before, so it would be awesome to hear what he used, his results, and any more information he could add. /forum/images/graemlins/smile.gif

Concerning your second question, coconut oil is an excellent source. And, yes, they would be excellent to have on a bulk-- especially if my research hypothesis is correct.

[Venom]

[ QUOTE ]

Would eating medium chain TGs actually inhibit to a certain degree your body's ability to burn fat it has stored? Or would it speed this up a bit?
I'm thinking, if your diet contains these fats that are more quickly oxidized, will your body use these up first (not taking into account carb oxidation), then call on fat stores for energy?

[/ QUOTE ]

It would speed it up for sure. As stated in the original post, one of the destinations of fats are to be stored themselves when digested. Having MCT’s decreases this probability, shifting the metabolism of fats towards its anabolic functions such as increasing diet induced thermogenesis and perhaps the production of anabolic hormones!

[ QUOTE ]

I would be interested to see an article that talks about the mechanism fat stores in the body are broken down for energy. At what point do they get tapped into?

[/ QUOTE ]

There are two factors to consider here: nutrient partitioning and total calories metabolized.

Nutrient Partitioning can be defined as the distribution of ingested nutrients among basal metabolism, growth, tissue maintenance and repair, physical activity, and other forms of energy expenditure and nutrient storage. The goal is to partition nutrients away from fat storage, and towards other vital functions such as replenishment of glycogen stores (which is the storage form of glucose, and the predominant source of energy used during high intensity exercise, such as weight lifting).

One of the most effective ways to do this is manipulation of the hormone insulin. Insulin is a hormone released from the beta cells in the islets of Langerhans of the pancreas. Its primary secretagogue (anything that stimulates the release of a hormone) is glucose. A primary importance of carbs is therefore, to manipulate this hormone.

Insulin has numerous anabolic effects such as increasing protein synthesis and glycogen replenishment. However, insulin also spares fat from being utilized as fuel, and chronic production of this hormone can increase de-nova lypogenic enzymes, increasing the probability of converting carbohydrates to fat for storage. Thus, it is important to use various methods to enhance insulin sensitivity.

What is important to understand is that chronic release of a hormone will promote down regulation. Receptors exposed to hormones to unphysiologically high concentrations, or for long periods of time, are down regulated (become less available for hormone action). Thus, by constantly having high Gi carbs for instance, insulin will be constantly released, causing down regulation.

One of the best ways to enhance insulin sensitivity is through exercise. Omega 3 fatty acids have also been shown to enhance insulin sensitivity, as well as dietary fiber.

Knowing the actions of insulin, this is why some people opt for carb cycling when they diet.

And there are numerous other ways you can manipulate your diet so that you minimize fat storage of ingested nutrients, such as having MCT’s.

Exercise is one of the most effective ways to manipulate this. Here is a quote from the current issue of JHR from Wilson (2005) The Growth Hormone – IGF Axis and its Role in Muscular Hypertrophy (http://www.abcbodybuilding.com/ghigfaxis.php)

[ QUOTE ]
In summary, during catabolic states, when muscles are taxed the body adapts by lowering IGF-1 levels, while local IGF-1 levels in the trained musculature increase. This creates systemic catabolism, while maintaining the possibility for local anabolism. Theintz (1993) suggests that this attenuates somatic growth while maintaining muscular adaptation during states of caloric restriction. These hormonal adaptations have been seen in both female gymnasts and wrestlers who enter states of catabolism during weight loss periods, while still maintaining or adding musculature in the trained regions (Jahreis et al., 1991, Roemmich and Sinning, 1997, Elokim et al., 2005). Finally, it also explains partially why periods of overfeeding facilitate a more whole body anabolic environment conducive to size increases.

[/ QUOTE ]

Therefore, by manipulating nutrient partitioning techniques, you can add muscle, and lose fat at the same time! The competitors of the HYPERplasia challenge are living proof of this.

Next, you obviously will need to metabolize calories. There are 3 primary avenues for this: Diet Induced Thermogenesis (DIT), Basal Metabolic Rate (BMR), and Exercise.

The president and I plan on writing an extensive article on DIT for the upcoming issue of JHR. But typically, this accounts for 10% of the calories you metabolize. DIT is the increase in the amount of calories metabolized caused by eating foods. This is entirely dependent on the type of foods you eat.

BMR is the basic energy requirements needed to maintain vital organs such as the liver and kidney, as well as muscles, which can obviously be manipulated and will greatly increase your BMR. Typically, this accounts for 65% of daily oxidative metabolism. So it is absolutely vital to maintain it. Dieting tends to decreases it, so this is why people utilize various methods such as carb cycling and calorie cycling.

The last one is exercise, and the amount of calories you metabolize through this avenue can obviously vary.

If you want to optimize the amount of calories you metabolize from fat during exercise, evidence suggests training at 65% of your VO2 max will metabolize the highest total amount of fat. For more information on this, read these articles by Wilson and Wilson (2005):

Fast Acting Hormones and their Role in Fuel use during Exercise

Slow Acting Hormones and their Role in Fuel use during Exercise

Analysis of Nutrient use during Low, Moderate, and High Intensity Exercise

Direct Comparisons of Fuel use during Low, Moderate, and High Intensity Exercises

Here. (http://www.abcbodybuilding.com/anatomyexecise.php?id=18&subId=49)

[TheShanMan]

[ QUOTE ]
Wilson, G (2003) covered polyunsaturated fats extensively in his EFA article.

[/ QUOTE ]
I got a good chuckle when I read how you referred to yourself as "Wilson, G" and "his" here. /forum/images/graemlins/grin.gif

[Venom]

haha, I enjoyed writing that. /forum/images/graemlins/grin.gif

[psaturn]

I have a link with coconut oil used for control of obesity:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9806312&dopt=Citation

1: Int J Obes Relat Metab Disord. 1998 Oct;22(10):974-9. Related Articles, Links

Energy restriction with high-fat diet enriched with coconut oil gives higher UCP1 and lower white fat in rats.

Portillo MP, Serra F, Simon E, del Barrio AS, Palou A.

Nutrition and Food Science, University of Basc Country, Vitoria, Spain.

OBJECTIVE: To investigate the effects of overfeeding on a high fat diet, enriched in coconut oil, and the influence of food restriction on the uncoupling protein (UCP1) expression and on body fat content. DESIGN AND SUBJECTS: In experiment I, female Wistar rats were fed ad libitum either a normal-fat diet (control group, C) or a high-fat diet (HF), enriched in coconut oil, for 7 weeks. In experiment II, HF rats after finishing experiment I were fed (for 3 weeks) either the normal-fat diet (group CAHF, Control After High Fat) or food restricted diets which provided 60% of the energy intake of group CAHF: a group fed a low-energy, normal-fat diet (LENF) and another fed a low-energy, high-fat diet (LEHF). MEASUREMENTS: Body and fatty depot weights. Food intake. Protein and UCP1 levels of interscapular brown adipose tissue. RESULTS: High-fat diet feeding promoted an increase in body fat content, body weight and UCP1 levels. Energy restriction induced similar body weight reduction in groups LENF and LEHF. However, some adipose depots were more strongly reduced in the rats fed the high-fat diet enriched in coconut oil (group LEHF) than in the rats fed the normal-fat diet (Group LENF). Specific UCP1 was 2.0 (group LENF) and 3.4 (group LEHF) times higher than in controls (group CAHF). CONCLUSION: The coconut-oil enriched diet is effective in stimulating UCP1 expression during ad libitum feeding and in preventing its down regulation during food restriction, and this goes hand in hand with a decrease of the white fat stores.

[Grimm932]

thanks so much for your response Venom, I appreciate you taking time to share your knowledge. Some follow up questions regarding the coconut oil:

Is there any specific brand of coconut oil you recommend? I have noticed some are classified "virgin" and some "extra-virgin". Does it matter which one I take? Also would I consume coconut oil in one of my protein/fat meals (towards the end of the day) substuiting another fat source (such as walnuts or flax oil) with the coconut oil? Or would I have have it earlier in the day in one of my protien/carb meals and replace brown rice or oats with the coconut oil? Also, should I just consume it by itself (like flax oil) or can I actually use it to cook/bake/etc.? Also does coconut milk offer the same benifits as the oil? Sorry for the barrage of questions and thanks again for your help.

OldSchool, I would really like to hear about your experiences with adding sources of saturated fats in your diet. What specific sources (and what amounts) did you use? What benefits did you feel it provided to your bulk? And also I would love to hear what other information and knowledge you posses regarding this topic. thanks a lot!

[book]

I was re-reading the original post and just though of 2 more questions

1) A lot of the studies showed how a lower fat intake (such as going from 40% to 20% of total calories comming from fat) had a lower amount of anabolic hormones. So, generally, do you think fats could be upped to as much as 25-35%?

2) When steak was mentioned I thought of how back in the day Arnold and all those bodybuilders were still eating high fat cuts of red meat and plenty of whole eggs. Are these natural sources mainly constituted of MC triglyceride type saturated fats? and junk food like Mcdonalds comprised of longer chain fats?

[stillflabby]

thank you very much for the post Venom.

that cleared things up a lot for me. I haven't read the suggested reading yet, but it's in the queue.

All this will help me better understand what and why I'm doing things to burn fat...and I've got a lot to burn.

I ordered a set of calipers today to help me keep track of progress.

[littleamazon]

Ok...you guys are awesome!
I have no clue what else to say.

Amazon

[Venom]

[ QUOTE ]
Ok...you guys are awesome!
I have no clue what else to say.

Amazon

[/ QUOTE ]

Indeed, I am THRILLED with your guy’s feedback! You guys are developing into great scientists. /forum/images/graemlins/grin.gif

Great article, Psaturn, thank you. /forum/images/graemlins/smile.gif

Hi, Grimm

[ QUOTE ]

Is there any specific brand of coconut oil you recommend?

[/ QUOTE ]

Nope, either one should be fine. But I am still investigating all the sources we can get this from.

[ QUOTE ]
Also would I consume coconut oil in one of my protein/fat meals (towards the end of the day) substuiting another fat source (such as walnuts or flax oil) with the coconut oil

[/ QUOTE ]

That is what I would do. Just make sure you are having the minimal amount of EFA’s I advised in my article.

[ QUOTE ]
Also, should I just consume it by itself (like flax oil) or can I actually use it to cook/bake/etc.?

[/ QUOTE ]

You can cook with it.

[ QUOTE ]
Also does coconut milk offer the same benifits as the oil?

[/ QUOTE ]

Well, it is not as dense in MCT’s, but those that are in it will help.

[ QUOTE ]

OldSchool, I would really like to hear about your experiences with adding sources of saturated fats in your diet. What specific sources (and what amounts) did you use? What benefits did you feel it provided to your bulk? And also I would love to hear what other information and knowledge you posses regarding this topic. thanks a lot!

[/ QUOTE ]

Me, too! /forum/images/graemlins/laugh.gif

[Brad22]

I have some muscle milk which has a fair amount of mcts but have been avoiding due to this high saturated fat content of it. Would this make it acceptable to eat on my next bulk so I dont feel like i wasted the money or is it still unacceptable

[Venom]

It is still unacceptable.

Muscle milk does a switch and bait. They include one good ingredient—MCT's—and the rest is garbage.

[Venom]

No problem, stillflabby. I hope you get the results you desire. /forum/images/graemlins/smile.gif

Hey again, book /forum/images/graemlins/smile.gif

[ QUOTE ]

1) A lot of the studies showed how a lower fat intake (such as going from 40% to 20% of total calories comming from fat) had a lower amount of anabolic hormones. So, generally, do you think fats could be upped to as much as 25-35%?

[/ QUOTE ]

Yes. It depends on the diet, though. I think on a cut, going around 35% would be a great idea—especially when low carb dieting.

On a bulk, you still want to include an ample amount of fats, but your percentage will naturally go down, due to higher carbohydrate intakes.

I started implementing a higher fat diet, and lowered my carbs a bit more during my cut, and I notice a HUGE difference. I have a much better feeling of well being, have bigger pumps, and my capacity to express various skills in the weight room are pretty much as good as my last bulk. And I have been cutting for over 8 weeks, am doing hours of cardio weekly, and am pretty much carb depleted. I have done this for the past two weeks, and this is the best results I have gotten so far on my cut for my energy, body composition, and lifts. /forum/images/graemlins/smile.gif

[ QUOTE ]

2) When steak was mentioned I thought of how back in the day Arnold and all those bodybuilders were still eating high fat cuts of red meat and plenty of whole eggs. Are these natural sources mainly constituted of MC triglyceride type saturated fats? and junk food like Mcdonalds comprised of longer chain fats?

[/ QUOTE ]

No, steak is low in MCT’s.

[stillflabby]

[ QUOTE ]

Yes. It depends on the diet, though. I think on a cut, going around 35% would be a great idea—especially when low carb dieting.

On a bulk, you still want to include an ample amount of fats, but your percentage will naturally go down, due to higher carbohydrate intakes.

I started implementing a higher fat diet, and lowered my carbs a bit more during my cut, and I notice a HUGE difference. I have a much better feeling of well being, have bigger pumps, and my capacity to express various skills in the weight room are pretty much as good as my last bulk. And I have been cutting for over 8 weeks, am doing hours of cardio weekly, and am pretty much carb depleted. I have done this for the past two weeks, and this is the best results I have gotten so far on my cut for my energy, body composition, and lifts.


[/ QUOTE ]

This is very surprising to me. Makes me think of a healthy version of the Atkins diet. Except instead of eating 3 pounds of bacon, you take in healthy fats and protein.

I've edited this post, I asked about your sources of fats, then I remembered the article on EFAs. http://abcbodybuilding.com/efa.php

I was happy to see sardines on the list...I eat those daily. In fact, I'm about to have those now with some cottage cheese. mmmmmm

[stillflabby]

[ QUOTE ]
I started implementing a higher fat diet, and lowered my carbs a bit more during my cut, and I notice a HUGE difference. I have a much better feeling of well being, have bigger pumps, and my capacity to express various skills in the weight room are pretty much as good as my last bulk. And I have been cutting for over 8 weeks, am doing hours of cardio weekly, and am pretty much carb depleted. I have done this for the past two weeks, and this is the best results I have gotten so far on my cut for my energy, body composition, and lifts

[/ QUOTE ]

I don't understand when exactly you are carb depleted. Is it for this entire 2 week cycle? Or just during the workout? I like the idea of being carb depleted during cardio though. Seems like it would really promote ketosis for fuel.

The way I read it I'm not sure. I presume it's just during the workout, as ketosis for 2 weeks could be dangerous. But I'm not sure if the supplements you take are enough to counter act the higher acidity levels in the blood.

[Venom]

Hey, bro

No, I am not doing anything like atkins. I always have my post workout shake, which contains lots of carbs, and I also have carbs for breakfast; however, I have lowered my dosages in those meals. The rest of the day, I have primarily been having leafy greens. The biggest difference is that I have upped my fats, but I am not stuffing myself at all. A typical meal may consist of 1 spoon full of flax, some eggs, and whey protein.

Also, I am carb cycling. I have a high carb day every 2-3 days. That includes tomorrow! /forum/images/graemlins/grin.gif

[Endless]

[ QUOTE ]

Also, I am carb cycling. I have a high carb day every 2-3 days. That includes tomorrow! /forum/images/graemlins/grin.gif

[/ QUOTE ]

Good planning, Venom! Can't wait to eat!
Sorry, I'm being a trouble-maker...
-endless

[Venom]

lol, I was hoping you were coming! I need your help with my forearm! /forum/images/graemlins/grin.gif

[Grimm932]

hi, thanks Venom for your response. I did some research on the internet about MCTs and coconut oil and from what I have gathered it seems that while coconut oil is probably the best natural food source for MCTs, they are really not all that optimal because about half of their saturated fat is slightly longer chain (c-12) type, with only about a quarter in the c-6 to c-10 range. From what I read, this is the optimal range, with c-8 being the most beneficial. It seems to really be getting a good amount of MCTs one would have to use a pure MCT oil supplement, most of which contain 90+ percent of their saturated fat in the c6 - c10 range. What do you think? Are there other benifits to coconut oil that pure MCT oil does not offer (specifically does c-12 provide any benifits)? Thanks again so much for your help.

[Venom]

Incredible research, Grimm!!!!!!!


I am going to have to do some more investigation before commenting, but you have given me some excellent ideas on issues to look for. If there is not an optimal product for this, or if only a certain type of MCT is optimal (i.e. c8) then I could try to propose a formula for Champion to make for us. /forum/images/graemlins/laugh.gif

[John Black]

I'd just like to add that any experimental stuff you guys have to do, whether it be humane or otherwise, The John Black is your lab rat. Feel free to open my head and pull stuff out if you have to, or better yet, put stuff in. haha

BTW, excellent information!

[Venom]

HAHAHA! Thanks, John. /forum/images/graemlins/grin.gif

[Grimm932]

Wow I am really learning a lot through this thread. Thanks for always responding so promptly.

Well in terms of there being products that consist of MCTs mostly in the c6 - c10 range, it seems that that is exactly how most of the products are formulated.

For example: the SciFit MCT oil has the following properties... Ingredient Details:
*MCT Oil: 27g (medium chain triglycerides) Approx. Carbon Chain Distribution- C6: 3% max, C8: 65-85%, C10: 23-33%, C12: 3% max

source: http://eworldsupplements.com/products.php?p=104047

Another MCT Oil product (found here: http://www.iherb.com/mctoil.html) states that it is "is concentrated in 8-carbon length caprylic acid and 10-carbon length capric acid in a blended ratio of approximately 2 to 1" which means it is pretty similar to the Sci-Fit product.

Universal Nutrition also makes a pure MCT oil product which has pretty much the exact same ratio.

So it seems like it would be much more optimal to supplement with MCTs using an MCT oil product rather than coconut oil, which is much less concentrated in the type that are of the most benifit.

Well I really am looking forward to your investigation on this topic and what conclusions you come to. I find this subject quite fascinating and thanks for helping me, and others here at the forum, build on our knowledge.

[Grimm932]

Here are the details about the Ultimate Nutrition MCT oil: http://eworldsupplements.com/products.php?p=104049

[Venom]

FANTASTIC research, Grimm. I am very impressed. Thanks a lot for sharing that information. /forum/images/graemlins/smile.gif

So are you going to start using one of those oils? If so, share your results!

[Venom]

Thanks again everyone for your feedback. I am going to work on an article for this soon!

I will make the next research question of the week shortly. /forum/images/graemlins/smile.gif

[Leafy Green Vegetables]

[ QUOTE ]
Hey, bro

No, I am not doing anything like atkins. I always have my post workout shake, which contains lots of carbs, and I also have carbs for breakfast; however, I have lowered my dosages in those meals. The rest of the day, I have primarily been having leafy greens. The biggest difference is that I have upped my fats, but I am not stuffing myself at all. A typical meal may consist of 1 spoon full of flax, some eggs, and whey protein.

Also, I am carb cycling. I have a high carb day every 2-3 days. That includes tomorrow! /forum/images/graemlins/grin.gif

[/ QUOTE ]

Would you still include starchy carbs in PWO meal to regulate insulin?

[Venom]

I was for most of my cut, but the last several weeks I have been going very low carb for a shock, since I am almost done with this cut. I have just been having a lot of cabbage, instead. /forum/images/graemlins/grin.gif

[Leafy Green Vegetables]

[ QUOTE ]
I was for most of my cut, but the last several weeks I have been going very low carb for a shock, since I am almost done with this cut. I have just been having a lot of cabbage, instead. /forum/images/graemlins/grin.gif

[/ QUOTE ]


Thanks for the reply! Cabbage?....Nasty. /forum/images/graemlins/tongue.gif

[Damien Voorhees]

Great thread!

I have an observation that may be of interest. My son and I were in Italy last summer. It was very easy to pick out Americans from Italians. It wasn't the clothing or the language. The only overweight and often obese people were Americans. They stood out as sore thumbs! Even very old people looked very healthy, except for their cigarettes!

There are next to no fast food joints in Italy, and rarely a McDonalds. In fact, the only way McDonalds was allowed to open in Italy was if they offered good foods on their menu.

Italians typically eat what is called the Mediterranean diet: 40% of calories come from olive oil [mono-unsaturated] and they eat smaller portions of red meat than Americans, plus more seafood.

At e-diets, they are touting the Mediterranean diet:

Our Mediterranean plan will help you follow a diet similar to that traditionally found in the countries around the Mediterranean. This plan is rich in healthy fats from fish, olive oil, nuts and seeds, and you'll find plenty of fresh fruit and vegetables here, too. This diet is a rich source of essential fatty acids and antioxidants, a combination which can help improve cholesterol levels and protect heart health.

Anecdotal evidence can often give great clues as to where to begin doing research. Perhaps a modified Mediterranean diet with bodybuilding in mind could be a start for a research study.

[ryancostill]

[ QUOTE ]

Anecdotal evidence can often give great clues as to where to begin doing research.

[/ QUOTE ]

A great point.

INteresting insight into the meditteranaen diet. I visited Italy this summer too and I was also struck by the lack of fast food joints, a very refreshing change. They have an insane amount of icecream joints though!!

[Venom]

Good post, Damien.

Yes, it is really interesting to study habits of other countries, and then measure obesity and fitness levels. If you look at many other countries, they are all so active, too.

One of the biggest things that have appeared to cause a problem is technology. It makes us so lazy AND stressed. With the internet, peoples worloads are often way harder than if it did not exist, because of the massive amounts of emails they get, for instance. And with technology, we don't have to walk or bike anywhere; instead, we just drive. This is the opposite in many countries--often, by choice. There are many other examples, too.

I think it brings up a good point, too. Bodybuilding is not just a sport, it is a life style. If we are really going to change the health of our society, we need to make life style changes. This means changes in accessibility to fast food restaurants, changes in transportation, changes in various technologies that cause us stress, etc. Interesting issues to ponder!

[ryancostill]

[ QUOTE ]

One of the biggest things that have appeared to cause a problem is technology. It makes us so lazy AND stressed. With the internet, peoples worloads are often way harder than if it did not exist, because of the massive amounts of emails they get, for instance. And with technology, we don't have to walk or bike anywhere; instead, we just drive. This is the opposite in many countries--often, by choice. There are many other examples, too.


[/ QUOTE ]

Very good point. Often the obesity epidemic in the USA is blamed on the huge number of fast food chains. While these definately contribute they cannot be the sole factor. You make an interesting point saying [ QUOTE ]
we don't have to walk or bike anywhere; instead, we just drive. This is the opposite in many countries--often, by choice.

[/ QUOTE ]. this is very true. Amercia is such a "motor" country. By that I mean the country is very spread out and not really designed for pedestrians or cyclists. It is a country designed for the automobile. (this is just my own opinion... having lived in Maryland, New York and visted much of the west coast and Boston, Mass). Compare this to countries such as Denmark, and Holland, which are economically and technologically similar to the USA but where cycling is hugely encouraged and used as means of transport. In thiese countries you will see literally thousands of people cycling on the streets each morning. And in these countries, to my knowledge, obesity is not as much of a problem.

Note: this is also not to say that the USA is the only country with an obesity epidemic, it was just an example there are many others.

[Damien Voorhees]

There is gelato everywhere in Italy but perhaps that's their only vice! Well, of course, there is the wine! /forum/images/graemlins/smile.gif

[ryancostill]

Ok, quick question about MCT sources. You mentioned that Coconut Milk is not as dense in MCTs as coconut oil, but is it still a good source? How much of the saturated fat in coconut milk is MCTs? For example, my coconut milk contains 17g of Fat per 100ml. 16.8g of this is saturated fat. How much of this saturated fat is from MCTs? How much of it is longer chains which may cause fat deposition or higher cholesterol?

[sucramdw]

[ QUOTE ]
Ok, quick question about MCT sources. You mentioned that Coconut Milk is not as dense in MCTs as coconut oil, but is it still a good source? How much of the saturated fat in coconut milk is MCTs? For example, my coconut milk contains 17g of Fat per 100ml. 16.8g of this is saturated fat. How much of this saturated fat is from MCTs? How much of it is longer chains which may cause fat deposition or higher cholesterol?

[/ QUOTE ]

10oz of coconut milk is equivelent to roughly 3 1/2 tbsp. of coconut oil. Coconut oil is roughly 92% saturated fat, 6% monounsatured fat, and 2% polyunsaturated fat. Of that 92%, 64% is MCFA's. Coconut oil is the richest source for MCFA's, with the second being Palm Kernal Oils at 58%.

[ryancostill]

Thanks for the reply bro.

Ok, so if 10oz is = to 3 1/2 tbsp of oil, what else is in coconut milk? Is there harmful filler? or is it just water? ie. if there is nothing extra in it, the oil is just more condensed?

for those who use metric like me, 10oz = 300ml.

[**DONOTDELETE**]

I found this interesting article on web about MCT!!

http://www.pedresearch.org/cgi/content/full/55/6/921

Regulation of Pancreatic Lipase by Dietary Medium Chain Triglycerides in the Weanling Rat
RUTH Z. BIRK and PATSY M. BRANNON

The Institute of Applied Biosciences, Department of Biotechnology Engineering [R.Z.B], Ben-Gurior University, Beer-Sheva, 84105, Israel; and Department of Nutrition and Food Science [P.M.B.], University of Maryland, College Park, Maryland 20742, U.S.A.

Correspondence: Ruth Birk, Ph.D., The Institute of Applied Biosciences, Department of Biotechnology Engineering, Ben-Gurion University, P.O. Box 653, Beer-Sheva 84105, Israel; e-mail: rbirk@bgumail.bgu.ac.il


ABSTRACT
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

Pancreatic lipase (PL) and its related protein 1 (PLRP1) are regulated by the amount of dietary fat through an apparent transcriptional mechanism. Regulation of PL and PLRP1 by type of fat (chain length and degree of saturation) is less well understood. The aim of this study was to determine whether medium-chain triglycerides regulate PL and PLRP1. For 7 d, weanling (21-d-old) Sprague Dawley male rats were fed diets low (11% of energy), moderate (40% of energy), or high (67% of energy) in trioctanoate/tridecanoate (MCT) or safflower (low fat only) oils. Food consumption decreased as dietary MCT increased, and the consumption of MCT diets was lower than that of the low-safflower (control) diet. Final body weight was similar among rats fed the low- or moderate-MCT or control diets, but was significantly reduced (17%) in those fed the high-MCT diets. PL activity was significantly elevated 53–60% (p < 0.002) in rats fed low and moderate MCT diets, respectively, compared with that of rats fed high-MCT or control diets. PL and PLRP1 mRNA levels were not significantly different among diets, suggesting that chain length regulates PL and PLRP1 translationally or posttranslationally. The ß-hydroxybutyrate plasma concentration was significantly (p < 0.02) higher (85%) in rats consuming low-MCT diet compared with those of rats fed the control diet. MCT at low levels, but not high levels, increase PL activity without changing its mRNA levels.

Abbreviations:
MCT, medium-chain triglycerides
PL, pancreatic lipase
PLRP1, pancreatic lipase related protein 1
PLRP2, pancreatic lipase related protein 2
LCT, long-chain triglycerides


INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

Pancreatic lipase (PL) is the main enzyme responsible for digestion of dietary triglycerides. PL catalyzes the hydrolysis of 56% of the fatty acids of dietary triglycerides, and gastric lipase, an additional 10% (1). PL and its related protein PLRP1, a homologous protein of unknown function (2), are secreted by the pancreas and regulated by dietary fat (3–5). Considerable amount of work has been reported about the dietary regulation of PL by triglycerides, but many of the studies before 1994 used a cDNA probe initially believed to be PL and subsequently shown to be PLRP1 (2). PL was initially cloned by Lowe and co-workers (6) and referred to as rat PL3 by Wicker-Planquart and Puigserver (7). PL demonstrates the classical dependence on colipase for its lipolytic activity. PLRP1 (known before 1994 as pancreatic lipase 1/2) is highly homologous to PL (65%) (2, 8), but to date no known lipolytic activity of PLRP1 has been reported. Site-directed mutagenesis of two amino acids in PLRP1 to those seen in PL restores full colipase-dependent lipolytic activity of PLRP1, suggesting that PLRP1 may be a nonfunctional homologue of PL (9). Another homologue, pancreatic lipase related protein 2 (PLRP2) has 65% identity to PL and hydrolyzes triglycerides, phospholipids, and galactolipids. PLRP2 has low colipase dependence and does not exhibit bile salt inhibition as PL does (2, 8, 10, 11) . It is unknown whether PLRP2 is regulated by dietary fat.

The pancreas normally produces and secretes 3- to 10-fold excess lipase; therefore, the physiologic importance of regulating PL has been questioned. However, the dietary regulation of PL mediates the response of cholecystokinin (CCK) to dietary fat by increasing the efficiency of triacylglyceride digestion in the proximal small intestine (12). The enhanced release of fatty acids in the proximal intestine increases the responsiveness of CCK and causes a "feed forward" effect that coordinates the digestion of dietary triglycerides (12). Similarly, humans who consume a fat meal with orlistat (a lipase inhibitor) have accelerated gastric emptying and reduced CCK release and output of lipase, trypsin, and bilirubin (13). Thus, PL plays an important role in the regulation of gastric emptying and pancreatic and biliary secretion after ingestion of fat in humans.

The amount of fat in the diet regulates PL and PLRP1 expression (3, 14–16). When a high-fat diet is introduced to rats, PL protein synthesis and content and PLRP1 mRNA levels increase within 24 h (36%, 20%, and 412%, respectively) (14). After 5 d, PL content and synthesis and PLRP1 mRNA levels reach steady-state maximal levels (191%, 217%, and 650%, respectively) (14). The regulation of PLRP1 by the amount of dietary fat is transcriptional, as demonstrated by increased nuclear transcript run-on assay (15). The parallel changes in PL mRNA levels (16) and synthetic rates (14) suggest that the regulation of PL is pretranslational and likely to be transcriptional. However, such transcriptional regulation has yet to be conclusively documented.

The regulation of PL and PLRP1 by the type of fat (chain length and degree of saturation) is controversial. Deschodt-Lanckman and co-workers (17) report a higher increase in PL activity by diets high in unsaturated triglycerides compared with those high in MCT (tricaprylin). Saraux et al. (18) report that MCT (C:8–C:10) do not increase PL activity and total content compared with longer chain triglycerides. Sabb and co-workers (19) report that PL activity is regulated similarly by different types of fat above a threshold of 49% of energy. Below that threshold level, only the highly unsaturated safflower oil and coconut oil, which is rich in MCT, stimulate PL activity. Ricketts and Brannon (16) report that the amount of fat, independent of its degree of saturation, regulates PL pretranslationally, as increasing either saturated or polyunsaturated dietary fat results in parallel changes in PL and PLRP1 mRNA levels. However, the degree of saturation of dietary fat regulates PL at other levels as well. Translational or posttranslational regulation is suggested because the increase in PL mRNA in rats fed the moderate lard diet does not result in a greater PL activity. Thus, the regulation of PL and its related proteins by dietary fat has multiple mechanisms. Further, the amount of fat regulates PL independently from the degree of saturation of the fat.

The effects of chain length, particularly in the range of 8–10 carbon chain, on PL regulation remain controversial. MCT are used in some premature and newborn formulas because of their reported faster digestion and absorption (20–22). MCT are also used as a source of fat in processed foods and in nutrition therapy in medical conditions such as pancreatic insufficiency, malabsorption, parenteral nutrition, and weight loss (20–22). The mechanisms whereby MCT regulate PL and PLRP1 are unknown. The aim of this study was to investigate the regulation of PL mRNA and content by different amounts of dietary MCT in weanling rats.


MATERIALS AND METHODS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

Experimental protocol. Twenty male weanling Sprague Dawley rats (Charles River Laboratories, Wilmington, MA) were housed individually in hanging cages in a temperature-controlled (24°C) environment with a 12:12-h light-dark cycle. Weanling rats were selected as a model of normal fat digestion in the postnatal period. The protocol was approved by the University of Maryland Animal Care and Use Committee, and the National Research Council’s Guide for Care and Use of Laboratory Animals was followed. Rats were weight matched into four groups(n = 5 per group) so that the average initial weight was comparable: 46.8, 47.0, 46.6, 47.2 (g) for low-, moderate-, and high-MCT and low-safflower diet, respectively. The rats were fed for 7 d ad libitum purified low- (LF; 11% of energy), moderate- (MF; 40% of energy) and high- (HF; 67% of energy) fat diets with MCT (trioctanoate/tridecanoate, Neobee 1053, Stepan, Maywood, NJ) or low-fat (11% of energy) diet with safflower oil (control). The period of 7 d was selected because maximal adaptation and new steady-state levels are seen in PL content, synthesis, and mRNA levels after 5 d (14). The composition of the diets is shown in Table 1. These diets were isonitrogenous (either by percentage of weight or percentage of energy) and isoenergetic, but varied in content of cellulose, which has been shown not to affect the exocrine pancreas (23). Food consumption was measured daily, and body weights were measured on the first and last day of the experiment. On d 7, the rats were euthanized by CO2 inhalation. Blood was drawn and frozen at –80°C for ß-hydroxybutyrate analysis. Pancreata were removed, and a portion was frozen immediately on dry ice and stored at –80°C for enzyme analysis. The remainder of the pancreas was used immediately for RNA isolation as described below.


View this table:
[in this window]
[in a new window]
Table 1. Dietary composition*

Pancreatic enzyme analysis. Pancreatic fragments were homogenized in nine volumes of PBS (PBS; 0.15 M NaCl, 5 Mm PO4, pH 7.4) with a Polytron homogenizer (Brinkmann Instruments, Westbury, NY, U.S.A.). Homogenates were centrifuged at 14,000 g at 4°C for 30 min. The supernatant was removed and soybean trypsin inhibitor was added (final concentration 0.01%). Lipase activity of the supernatant was assayed by a titrimetric method (19) with 20 mM NaOH using a gum arabic–stabilized emulsion of neutralized triolein with excess crude colipase. Lipase activity was expressed as units (micromoles FA released) per milligrams protein. Protein content of the supernatant was determined by the method of Lowry et al. (24), using bovine albumin as a standard.

ß-hydroxybutyrate plasma levels. ß-hydroxybutyrate levels were measured using Sigma Chemical kit 310-A (Sigma Chemical Co., St. Louis, MO, U.S.A.) (25).

RNA extraction and hybridization studies. RNA was isolated as described by Chomczynski and Sacchi (26). This method is a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture. Freshly isolated pancreatic fragments were immediately homogenized with a Polytron homogenizer (titanium probe) for 2 x 20 s in ice-cold 4 M guanidinium thiocyanate, 26 mM sodium citrate, pH 7, 0.5% sarcosyl, and 0.7% 2-mercaptoethanol. Sequentially, the RNA was extracted by adding 0.2 M sodium acetate (pH 4) and phenol and chloroform-isoamyl alcohol mixture (49:1). RNA was precipitated with isopropanol, reprecipitated with 75% ethanol, and dissolved in sterile diethyl pyrocarbonate (DEPC)-treated water. RNA was quantitated by UV absorption at 260 nm. The integrity of RNA was checked by 0.8% agarose gel electrophoresis for the presence of intact 18S and 28S ribosomal RNA.

Recombinant plasmids used in these studies were the generous gifts of Dr. H.F. Kern, University of Marburg, Germany (PLRP1 cDNA; 0.82-Kb insert in Pst I site of pUC9) (27); Dr. J. Williams, University of Michigan (PL cDNA; 1.5-Kb insert in EcoR I site of pUC18) (28); D. Soprano, Temple University, Philadelphia (28S cDNA probe); and Dr. P. Howells (PLRP2 cDNA; 1.3-Kb insert in XdaI and KpNI site in pKSII) (29). Previously, we reported negligible cross-hybridization of LPL and PLRP1 (30). We also examined the specificity of the homologous and heterologous hybridization of random prime-labeled PL, PLRP1, and PLRP2 cDNA inserts with 0.2 µg of linearized plasmid DNA containing PLRP2 insert. Hybridization and washing conditions were identical to those described here. The PLRP2 cDNA cross-hybridization to PL and PLRP1 plasmid averaged 0 and 0.1%, respectively, of its hybridization to the homologous PLRP2 plasmid. These results demonstrate the specificity of the hybridization of each PL probe under the highly stringent conditions used in this study. We have previously shown that rPL and PLRP1 do not cross-hybridize (<3%) (29). Specific mRNAs were quantitated by dot-blot hybridization within the range of linear hybridization (30).

Total RNA was diluted in DEPC-treated water to the appropriate concentration verified by absorbance at 260 nm. For denaturation, the samples were mixed with 6.15 M formaldehyde in 0.75 M NaCl and 0.075 M trisodium citrate (5x SSC; 1x SSC is 0.15 M NaCl and 0.015 M sodium citrate, pH 7) and heated for 15 min at 65°C. A within-filter control sample was spotted on each filter. The denatured samples were spotted onto a nitrocellulose filter using a Schleicher & Schuell (Keene, NH, U.S.A.) dot-blot apparatus. The filters were cross-linked by UV radiation with optimal dosage (120 mJ/cm2) and prehybridized at 42°C for 2 h in a solution containing 50% formamide 5x SSC, 5x Denhardt’s solution, 0.1% SDS, and 100 mg tRNA. Hybridization was performed at 42°C for 16–18 h after adding 32P-labeled cDNA probe. Plasmids containing cDNA inserts were labeled by nick translation for 28S and by random priming for PL and PLRP-1 (Promega labeling kits Prime-a-Gene and Nick translation; Promega, Madison, WI, U.S.A.). After hybridization, filters were washed under increasingly stringent conditions (2x SSC with 1% SDS to 0.2x SSC with 1% SDS). The films were autoradiographed overnight at –80°C. Autoradiographic films were quantitated by an area laser densitometer (Bio-Rad, Hercules, CA, U.S.A.) and volume integration. The data were expressed as relative absorbance units of each sample relative to the absorbance of 28S RNA.

Data analysis. All data, expressed as mean ± SE, were analyzed by one-way ANOVA and least significant difference (LSD) (31). Results were considered significantly different if p < 0.05.


RESULTS
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Food consumption and body weight. Food consumption was lower (p < 0.002) in rats fed HF-MCT diet (Table 2) compared with those fed LF-MCT (24%) and MF-MCT (20%) or LF-safflower (29%) groups. Food consumption was comparable in the LF-safflower and LF-MCT groups and also in the LF-and MF-MCT groups. Body weight was comparable among the LF-safflower and MCT and the MF-MCT groups (Table 2), but was significantly reduced (p < 0.02) in the HF-MCT group compared with the rats fed LF-safflower, LF-MCT, and MF-MCT diets (13–17%).


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Table 2. Effect of MCT on food and total fat consumption and final body weight

PL activity. PL activity (U/mg protein) was significantly elevated (p < 0.002) in rats fed LF- and MF-MCT diets compared with those fed LF-safflower diet (153% and 160%, respectively). However, rats fed HF-MCT diet had comparable PL activity to those fed LF-safflower diet (Fig. 1). Pancreatic weights were not different among the experimental groups. Average pancreatic weights were: 0.42 ± 0.05, 0.39 ± 0.04, 0.42 ± 0.03, and 0.42 ± 0.048 (g) for LF-, MF-, and HF-MCT and LF-safflower–fed rats, respectively.



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Figure 1. Effect of MCT on PL activity (U/mg protein). Weanling Sprague Dawley rats were fed for 7 d diets with LF- (11% of energy), MF- (40% of energy), or HF-MCT (67% of energy) or low-fat safflower (control) diets. Results are expressed as mean ± SE (n = 5 per group). *Values with superscript differed significantly from values without superscript (p < 0.002) by ANOVA and LSD.


mRNA levels. PL mRNA levels were comparable in rats fed LF-safflower or LF-, MF-, and HF-MCT diets (Fig. 2). PLRP1 mRNA levels were also comparable between rats fed LF-safflower or LF-, MF-, and HF-MCT diets (Fig. 2). PLRP1 mRNA levels were lower than PL mRNA levels, as has been reported before (2) because of the anti-coordinate developmental pattern of PL and its related proteins in the rat. The mRNA levels of PLRP-1 and PLRP-2 are low throughout weaning and adulthood, whereas PL expression is high at weaning and adulthood (2). PLRP2 mRNA levels were not detectable in any of the total RNA samples from LF-safflower or LF-, MF-, and HF-MCT–fed rats (data not shown).



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Figure 2. (A) PL mRNA/28S RNA ratio. (B) PLRP1 mRNA/28S ratio. Weanling Sprague Dawley rats were fed for 7 d diets with LF- (11% of energy), MF- (40% of energy), or HF-MCT (67% of energy) or low-fat safflower (control) diets. Results are expressed as mean ± SE (n = 5 per group). There was no significant difference among the groups, for either PL mRNA or PLRP1 mRNA.


ß-hydroxybutyrate plasma levels. The ß-hydroxybutyrate plasma concentration (mg/dL) was significantly higher (85%, p < 0.02) in LF-MCT–fed rats compared with those in rats fed LF-safflower or HF-MCT. The ß-hydroxybutyrate plasma concentration in rats fed MF-MCT was intermediate between its concentration in rats fed LF-MCT and LF-safflower (Fig. 3).



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Figure 3. Plasma ß-hydroxybutyrate (mg/dL). Weanling Sprague Dawley rats were fed for 7 d diets with LF- (11% of energy), MF- (40% of energy), or HF-MCT (67% of energy) or low-fat safflower (control) diets. Results are expressed as mean ± SE (n = 5 per group). *{dagger}Values not sharing a superscript differed significantly (p < 0.02) by ANOVA and LSD.



DISCUSSION
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ABSTRACT
INTRODUCTION
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DISCUSSION
REFERENCES

In this study, we describe significantly lower food consumption and final body weight in the rats consuming HF-MCT diet compared with those consuming LF- or MF-MCT and LF-safflower diets. Sabb et al. (19) found the same trend of decreased food consumption in rats consuming high-fat diets regardless of fat type. This trend in lower body weights (expressed as grams of weight gain per 100 Kcal intake per day) with high MCT was noted in premature babies fed formula containing 40% of the fat in the diet as MCT, who had higher weight gain than those fed formula containing 80% of the fat in the diet as MCT (32). Elevated levels of MCT in the diet are proposed to alter body composition, resulting in more lean tissue and less fat. Epididymal fat pads of rats fed high-MCT diets are smaller compared with those in rats fed long-chain triacylglycerides. Although the mechanism is not known, it is attributed to higher oxidation and enhancement of thermogenesis (22, 33). Despite the lower food intake by the HF-MCT group, the total fat consumed per day was increased in this group (2.7 g/d) compared with the LF-MCT and control groups (0.6 g/d; see Table 2).

In the present study, MCT at LF and MF levels elevated PL activity whereas MCT at HF levels did not affect PL activity. No previous study reports induction of PL activity by low levels of MCT, as this was not examined. High MCT (67% of energy) did not induce PL activity in our study in contrast to high long-chain fatty acids (67% of energy), which did induce PL activity in our previous study (19). However, increasing long chain fatty acids to 75% of energy in the diet diminishes the PL activity compared with that seen with 67% long-chain fatty acids (19). Further, a dietary ketone precursor, butanediol, also exhibited a biphasic effect on PL activity with increased PL activity by 7.5% and 14% butanediol but no change in PL activity by 28% (34). The biphasic response to MCT is congruent with the biphasic response to LCT and dietary ketones. Why such a biphasic response by PL occurs is unknown, but such a response may result from biphasic effects on the hormonal or metabolic mediators of this dietary regulation. Alternatively, another explanation of this biphasic response may be that MCT have a higher formation rate of emulsion particles and thereby enhanced hydrolysis by PL (35). The released medium-chain fatty acids (MCFA) may exert less allosteric inhibition on PL, and medium-chain 2-monoglycerides may isomerize more rapidly than those of long-chain length, thereby facilitating rapid hydrolysis (33). Such rapid hydrolysis might affect the regulation of PL through effects on either the release of secretin or gastric inhibitory polypeptide, proposed mediators of the dietary regulation of PL (36, 37), or the generation of ketones, another proposed mediator (38). MCT are known to be oxidized more readily than LCT and may generate greater amounts of ketone at lower levels. The generation of ketones from MCT could be further enhanced by a more rapid hydrolysis and uptake of MCFA. Plasma concentration of ß-hydroxybutyrate was also significantly higher in rats fed LF-MCT compared with rats fed LF-safflower in this study, whereas ß-hydroxybutyrate plasma concentration of rats fed MF-MCT was intermediate. This parallel pattern of ß-hydroxybutyrate plasma concentration and PL activity supports the proposed role of ketones in mediating the dietary regulation of PL and may explain the more robust response of PL to low amounts of MCT. In contrast, lipolysis of emulsified LCT may be inhibited by the soaps formed during the reaction and by their poor diffusion to the aqueous phase (39), which might result in less stimulation of the proposed mediators at lower dietary levels.

The lack of effect of high levels of MCT on PL has been reported by others. Saraux et al. (18) found that MCT did not increase PL content to the same extent as other fats, although they used only one high level of MCT in the diet (45% by weight). Furthermore, PL activity in their study was 67.3 U/mg of protein, which is very similar to the level we found at high dietary fat levels (31.6% by weight) of MCT (57.7 U/mg protein) in our study. Deschodt-Lanckman et al. (17) demonstrated a similar "poor induction" of PL in adult rats by 50% (by weight) of tricapric oil in the diet, but PL activity reached the same levels as we found in high levels of MCT diet (50 U/mg protein). Sabb et al. (19) demonstrated that increased dietary fat does not influence PL activity in a linear way; rather, PL activity response occurs past a threshold level of dietary fat and decreases beyond maximal levels (67% for corn oil). This decrease in PL activity occurs at a lower threshold when MCT is used as a fat source in the diet as described in this study.

The mechanism whereby MCT regulates PL appears to be translational or posttranslational, as PL and PLRP1 mRNA levels do not parallel the changes in PL activity. Our previous study (16) suggests that the degree of saturation of dietary fat regulates PL translationally or posttranslationally, because long-chain saturated and polyunsaturated triglycerides induced nonparallel changes in PL mRNA level and activity. The results of the present study also suggest that the amount of MCT also regulates PL translationally or posttranslationally because of the nonparallel changes in activity and mRNA levels. Further studies are needed to examine the effects of MCT on the synthesis, secretion, and degradation of PL.

Some studies emphasize the importance and advantages of using MCT in infant formulas: 1) higher rate of absorption, more rapid transport, and more efficient oxidation compared with LCT; 2) improved LCT absorption when combined with MCT; and 3) improved nitrogen and calcium absorption (32, 40–43). However, the use of MCT in formulas of premature infants and newborns has been questioned by others (44). High levels of MCT in the diet are not recommended because they may elevate the levels of circulating dicarboxylic acids and ketones (40). In previous studies, MCT-containing formulas were absorbed at a similar rate to LCT-containing formula when 50% of energy was MCT or LCT. Furthermore, the activity of gastric lipase is higher in formulas containing LCT compared with MCT (43, 45).

The present study demonstrates that MCT in the diet at low or moderate levels (11% and 40% of energy) elevates PL activity significantly in the weanling rat. This regulation of PL by MCT could be important for optimizing dietary triglyceride absorption by adjusting the MCT/LCT ratio to stimulate maximal PL activity and its "feed forward" coordination of fat digestion and avoid adverse effects of high levels of MCT in the diet.

The results of the present study strengthen the concern regarding the use of high levels of MCT in infant’s formula. Considering that LCT induces higher gastric lipase activity and that our results show higher levels of PL activity at low and moderate levels of MCT, it seems that lowering the ratio of MCT/LCT may be advisable.


ACKNOWLEDGMENTS

Supported by Maryland Agricultural Experiment Station 97–72 grants "Developmental and Dietary Regulation of Pancreatic Lipase." Trioctanoate/tridecanoate (Neobee 1053) was a gift of the Stepan Company, Maywood, NJ, U.S.A.


REFERENCES
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RESULTS
DISCUSSION
REFERENCES


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34. Shenoy S, Yager BK, Brannon PM 1998 Role of ketones in the regulation of pancreatic lipase by dietary fat. FASEB J 12: A514
35. Armand M, Borel P, Ythier P, Dutot G, Melin C, Senft M, Lafont H, Lairon D 1992 Effects of droplet size, triacylglycerol composition, and calcium on the hydrolysis of complex emulsions by pancreatic lipase: an in vitro study. J Nutr Biochem 3: 333–341[CrossRef]
36. Rausch G, Rudiger K, Vasilouds P, Kern HF, Scheele G 1986 Lipase synthesis in the rat pancreas is regulated by secretin. Pancreas 6: 522–528
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38. Bazin R, Lavau M 1979 Diet composition and insulin effects on amylase to lipase ratio in pancreas of diabetic rats. Digestion 19: 386–391[Medline]
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40. Lien EL 1994 The role of fatty acid composition and positional distribution in fat absorption in infants. J Pediatr 125: s62–s68[Medline]
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45. Hamosh M, Bitman J, Liao TH, Mehta NR, Buczek RJ, Wood DL, Grylack LJ, Hamosh P 1989 Gastric lipolysis and fat absorption in premature infants: effect of medium chain triglyceride or long chain triglyceride-containing formulas. Pediatrics 83: 86–92[Abstract]

Received for publication June 19, 2003. Accepted for publication February 16, 2004.

[**DONOTDELETE**]

Another article "Physiological Effects of Medium-Chain Triglycerides: Potential Agents in the Prevention of Obesity" is another interesting one.

http://www.nutrition.org/cgi/content/full/132/3/329

Recent Advances in Nutritional Sciences
Physiological Effects of Medium-Chain Triglycerides: Potential Agents in the Prevention of Obesity1
Marie-Pierre St-Onge and Peter J. H. Jones2

School of Dietetics and Human Nutrition, McGill University, Ste-Anne-de-Bellevue, Quebec, Canada, H9X 3V9

2To whom correspondence should be addressed. E-mail: jonesp@macdonald.mcgill.ca.

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Medium chain fatty acids (MCFA) are readily oxidized in the liver. Animal and human studies have shown that the fast rate of oxidation of MCFA leads to greater energy expenditure (EE). Most animal studies have also demonstrated that the greater EE with MCFA relative to long-chain fatty acids (LCFA) results in less body weight gain and decreased size of fat depots after several months of consumption. Furthermore, both animal and human trials suggest a greater satiating effect of medium-chain triglycerides (MCT) compared with long-chain triglycerides (LCT). The aim of this review is to evaluate existing data describing the effects of MCT on EE and satiety and determine their potential efficacy as agents in the treatment of human obesity. Animal studies are summarized and human trials more systematically evaluated because the primary focus of this article is to examine the effects of MCT on human energy metabolism and satiety. Hormones including cholescytokinin, peptide YY, gastric inhibitory peptide, neurotensin and pancreatic polypeptide have been proposed to be involved in the mechanism by which MCT may induce satiety; however, the exact mechanisms have not been established. From the literature reviewed, we conclude that MCT increase energy expenditure, may result in faster satiety and facilitate weight control when included in the diet as a replacement for fats containing LCT.

KEY WORDS: • medium-chain triglycerides • satiety • energy expenditure • obesity


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Fats varying in fatty acid chain lengths are metabolized differently (1Citation –8Citation ). Medium-chain triglycerides (MCT),3 containing 6–12 carbon fatty acids, differ from long-chain triglycerides (LCT), which have fatty acids of > 12 carbons, in that they are absorbed directly into the portal circulation and transported to the liver for rapid oxidation (1Citation ). LCT, however, are transported via chylomicrons into the lymphatic system, allowing for extensive uptake into adipose tissue. Therefore, it has been hypothesized that the rapid metabolism of MCT may increase energy expenditure (EE), decrease their deposition into adipose tissue and result in faster satiety. The objective of the present article is to review literature concerning the effects of MCT on EE, fat deposition and food intake as a means to establish the potential efficacy of MCT in the prevention of obesity in humans.


Effect of MCT on Energy Expenditure.
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Animal trials studying the effects of MCT vs. LCT consumption on lipid and energy metabolism have shown that body weight (BW) is reduced with MCT consumption compared with LCT consumption and that feed efficiency is thus reduced (9Citation –11Citation ). In a study in which rats infused with MCT gained one third of the weight gained by those infused with LCT, Lasekan et al. (9Citation ) concluded that replacing LCT with MCT over long periods could produce weight loss without decreasing energy intakes.

Human studies have mainly compared the effects of MCT vs. LCT in single-meal or single-day experiments. Scalfi et al. (3Citation ) evaluated the effects of a single mixed meal containing MCT on postprandial thermogenesis and examined possible differences in the thermic response between lean and obese men. Subjects consumed a meal containing 15% of energy from protein, 55% from carbohydrate and 30% from fat, in the form of corn oil (CO) and animal fat or MCT oil (56% octanoate, 40% decanoate) in random order. Energy expenditure measurements were conducted before and for 6 h after consumption of the meal. Total EE was 48 and 65% greater in lean and obese individuals, respectively, after MCT compared with LCT consumption. Similar results were obtained by Seaton et al. (4Citation ) comparing the effects of MCT or CO on EE after a single meal. Energy expenditure peaked at 16% above baseline after MCT consumption compared with 5% for CO.

Dulloo et al. (5Citation ) investigated the thermogenic effects of low-to-moderate amounts of MCT consumption in healthy adult men. Subjects were required to spend 24 h in a respiratory chamber on four separate occasions; during that time, diets differed in the ratio of MCT:LCT (0:30, 5:25, 15:15, 30:0) provided as added fat. The diet was given at a level 1.4 times energy requirements and the 30 g of added fat was distributed evenly across all meals. The authors found that EE between 0800 and 2300 h increased by 45, 135 and 265 kJ with 5, 15 and 30 g of MCT in the diet, respectively. Mean 24-h EE also increased by 162 and 475 kJ with 15 and 30 g of MCT in added fat, respectively. Thus, the greater effects of MCT than LCT on EE are evident not only in the few hours after the meal but for a much longer time.

Most results (3Citation –5Citation ) from single-day experiments indicated that replacing LCT for MCT in the diet could produce weight loss after prolonged consumption. However, when Flatt et al. (6Citation ) compared diets rich in MCT, LCT and low in fat, they concluded that a low fat diet was more prudent when aiming for weight loss. However, MCT consumption resulted in greater EE at several time points compared with the low fat diet.

Few trials have been conducted over longer periods. One of those studies examined energy balance during the overfeeding of liquid formula diets containing MCT (61% octanoate, 32% decanoate) or LCT (32% oleate, 51% linoleate) for 7 d (7Citation ). EE was measured on d 1 and 6 for 10–15 min every 30 min for 6 h after meal consumption. The thermic effect of food (TEF) was identified as 8% of ingested energy after MCT consumption compared with 5.8% after LCT consumption on d 1. After 6 d, TEF was 12 and 6.6% of ingested energy with MCT and LCT consumption, respectively, indicating that the difference in EE between MCT and LCT persists even after a week of overfeeding.

The study of longest duration (14 d) published to date (8Citation ) sought to determine whether fatty acid chain length influenced EE and substrate oxidation in women. Subjects consumed a controlled, weight maintenance diet containing 40% of energy as fat, either in the form of butter and coconut oil (MCT; 38.9% of fatty acids contained chains with <16 carbons) or beef tallow. Energy expenditure was measured before and for 5.5 h after breakfast. Postprandial total EE after MCT consumption was greater than after LCT consumption on d 7 but not d 14. The authors concluded that the effects of MCT consumption on EE may be transient.

All animal studies (9Citation –11Citation ) and most human studies (3Citation –5Citation ,7Citation ,8Citation ) have shown that MCT consumption increases EE compared with a meal containing LCT. Investigators who found the greatest differences also concluded that MCT could be used in the treatment or prevention of human obesity (3Citation –5Citation ). However, the studies conducted to date have been short, ranging from a single meal (3Citation –6Citation ) to several days (7Citation ,8Citation ). Whether effects of MCT on EE and RQ are long lasting and result in actual measurable and sustainable changes in body composition of humans remain to be established.


Effect of MCT on Fat Deposition.
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Given that feed efficiency studies in animals and energetic studies in humans indicate enhanced EE after MCT consumption (3Citation –11Citation ), additional work has examined whether increased EE translates into decreased fat mass. In animals consuming MCT, BW were lower, fat depots smaller (12Citation –15Citation ) and adipocyte size smaller (12Citation ,13Citation ) with MCT compared with LCT consumption. These results led the authors to conclude that MCT could potentially prevent (13Citation ) or control (15Citation ) obesity in humans. However, MCT consumption was not observed by Hill et al. (16Citation ) to cause greater weight loss than lard, CO or fish oil (FO). Body adipose tissue during the first 3 mo was not different among groups but after 6 mo, the group fed FO had less body fat than all other groups. Although both FO and MCT feeding resulted in small fat cells, only FO feeding was associated with inhibition of cell proliferation.

Only one study evaluated the ability of MCT to facilitate weight reduction in humans (17Citation ). Obese women (n = 16) consumed MCT (58% octanoate, 22% decanoate) or LCT (soy oil) in random order for either 4 wk if they were inpatients or 12 wk if they were outpatients, at a level of 191 kJ/d. There were no differences in weight loss or rate of weight loss between diet treatments. A liquid diet containing 24% of energy as MCT failed to increase the rate of weight loss compared with LCT. This lack of agreement with animal trials and EE experiments may have been due to the low fat content of the diets (1.5 g of total fat/d, of which 1.2 g was treatment fat) or to gender differences in the effects of MCT. Differences detected in EE with MCT and LCT consumption are considerably greater in males than females. When data are extrapolated from trials conducted in men (3Citation –5Citation ,7Citation ), average EE was ~460 kJ/d greater with MCT than with LCT consumption, with a peak difference between treatments of 669 kJ/d (7Citation ). In contrast, data from White et al. (8Citation ), who studied women, found differences in EE of 138 kJ/d between MCT and LCT consumption. Our own work with overweight women also revealed a difference in EE of ~188 kJ/d (18Citation ). From these preliminary data, it appears that women respond less readily to treatment with MCT than men.


Effect of MCT on Food Intake and Satiety. Animal studies.
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Lower weight gain and decreased fat depot size with MCT feeding compared with LCT feeding in animals have been attributed to two different effects of MCT, i.e., increased EE and decreased food intake. Satiety may also be affected by fatty acid chain length of dietary fat. Bray et al. (19Citation ) observed greater feed intake when LCT were included in the diets of the rats compared with diets containing MCT. After 80 d of consuming diets containing 60% of energy from CO, MCT or a mixture of the two, rats fed the CO and the CO-MCT diets had a higher BW than those fed the MCT diet alone. Rats fed the MCT diet consumed less energy, and the authors concluded that ß-hydroxybutyrate may play a role in the difference in food intake between MCT- and CO-fed rats.

Given these results, Maggio and Koopmans (20Citation ), in 1982, conducted a study to clarify the origin and the nature of the signals that terminate short-term food intake of mixed meals containing triglycerides (TG) with fatty acids of different chain lengths. Sprague-Dawley rats were intubated intragastrically and given free access to a liquid diet containing 21% of energy as fat. The TG infusions consisted of 70% TG (tributyrin, tricaprylin or triolein in different concentrations) and 30% carbohydrate. Shifting chain length from medium to long did not differentially affect food intake when the infusions were equicaloric. Therefore, the authors concluded that satiety may be related to the amount of energy ingested rather than to the physical characteristics of the specific nutrients. This was in contrast to results obtained by Denbow et al. (21Citation ) who infused intrahepatically or intubated intragastrically white leghorn ****erels with isoenergetic quantities of tributyrate, tridecanoate or trioleate and measured feed consumption. Feed consumption with SCT and MCT infusion was suppressed within 1 h after intrahepatic infusion until 180 min. However, when infusions were given intragastrically, only SCT decreased feed intake. The authors concluded that these results reflect the relatively rapid rate of digestion and absorption of short-chain fatty acids (SCFA) from the gut along with oxidation of SCFA by the liver.

Furuse et al. (22Citation ) also investigated the effects of two different levels of MCT on feed intake in rats. They further examined the capacity of endogenous cholecystokinin (CCK) to modulate feed intake with MCT. Feed intake of male Wistar rats fed diets containing CO, MCT or a 1:1 mixture of CO and MCT was determined every hour for 12 h and then at 2-h intervals for the following 12 h. In a separate trial, Devazepide (DVZ), a CCK-A receptor antagonist, was injected intraperitoneally 40 min before feeding and feed intake was measured at 1, 2, 3 and 6 h postinjection. Feed intake decreased in a dose-dependent manner with increased concentration of MCT in the diet and was enhanced 2 h after DVZ injection. After 3 h, intake of the MCT diet was less than that of the CO diet. The authors thus concluded that satiety is affected by carbon chain length in dietary TG sources.


Effect of MCT on Food Intake and Satiety. Human studies.
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If MCT consumption enhances satiety and decreases food intake in animals, an equivalent response might be expected in humans. Stubbs and Harbron (23Citation ) examined whether the effects of ingesting MCT can limit the hyperphagia associated with high fat, energy-dense diets in humans. Six men participated in a three-phase inpatient trial in which they had free access to experimental high fat foods (61.5% of energy as fat) for 14 d. Each experimental phase differed in the amount of MCT included in the diet, i.e., low, medium or high MCT content with 20, 31 and 40%, respectively, of total energy as MCT. Subjects consumed 15.1 and 17.6 MJ less with the diet containing the most MCT compared with the diets containing the low and medium amounts of MCT, respectively, over the 14-d period. Body weights during consumption of the low and medium MCT diets increased by 0.45 and 0.41 kg, respectively, and decreased by 0.03 kg with the high MCT content diet. Food and energy intakes were thus suppressed when two thirds of the fat content of a high fat diet was derived from MCT, but BW were not affected.

Another clinical trial (24Citation ) was designed to establish the influence of chain length and degree of saturation on food intake in normal-weight men. Breakfasts differing in the nature of the fat, i.e., olive oil, lard, MCT or a fat substitute, were served and food intakes at lunch and dinner were measured. Energy intake at lunch was lower after the MCT-containing breakfast than after all other breakfasts (3100 vs. 3715 kJ with the fat substitute, 3278 kJ with olive oil and 3798 kJ with lard) but there were no differences in food consumption at dinner.


Hormones Iinvolved in the Satiating Effect of MCT and LCT.
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Clinical trials (23Citation ,24Citation ) have shown that MCT consumption can lead to lower energy intakes but have not explored the underlying mechanism. More recently, research has focused on specific hormones that may be involved in the satiating effect of MCT. McLaughlin et al. (25Citation ) examined the relationship among fatty acid chain length, CCK secretion, and proximal and distal gastric motor function. Healthy volunteers (n = 15) were studied for their response to a control meal and orogastric infusion of 250 mL of a 0.05 mol/L fatty acid emulsion. Fatty acid emulsions containing fatty acids of 11 carbon chains and less did not increase plasma CCK concentrations compared with the vehicle, whereas long-chain fatty acids (LCFA) did. This study showed that the human proximal gut differentiates between fatty acid molecules; however, it does not support the role of CCK in mediating the satiating effect of MCT.

Several other studies have also reported that MCT do not stimulate CCK secretion in humans (26Citation –28Citation ), and trials have attempted to establish which hormone is responsible for the observed effects of MCT on food intake. Barbera et al. (26Citation ) compared effects of MCT and LCT on sensations of satiety, gastric tone, gastric inhibitory peptide (GIP), pancreatic polypeptide and CCK. Subjects (n = 9) were infused with saline, LCFA (mainly oleate and linoleate) or MCFA (octanoate and decanoate) on three separate occasions in random order. LCFA infusion resulted in a greater rise in satiation than MCFA, but there was no difference between the two fats on the perception of fullness and bloating. The rise in gastric volume was also greater with LCFA infusion than MCFA infusion. Similarly, LCFA increased baseline levels of plasma CCK, GIP, neurotensin and pancreatic polypeptide compared with saline, whereas MCFA infusion did not. The authors thus concluded that MCFA induce gastric relaxation without increasing satiation or plasma levels of gut hormones. However, because Stubbs and Harbron (23Citation ) and Van Wymelbeke (24Citation ) have shown lower food intakes with diets rich in MCT, it is likely that other factors play a role in regulating energy balance with MCT consumption.

Maas et al. (27Citation ) examined effects of MCFA and LCFA on peptide YY (PYY) release to determine whether PYY, which inhibits gastric acid secretion in humans, is involved in the enterogastrone effect of MCFA. These investigators had previously observed that infusions of MCFA suppressed gastrin-stimulated gastric acid secretion without the involvement of CCK (28Citation ). Men (n = 14) were intraduodenally infused for 2.5 h with MCFA (56% octanoate, 43% decanoate), LCFA (CO) or saline in random order. The energy loads differed between MCFA and LCFA infusions, with the former providing a load of 11.6 kJ/min and the latter providing a load of 22.7 kJ/min. Both infusions increased plasma levels of PYY; however, LCFA resulted in a greater increase than MCFA infusion (10.3 vs. 2.8 pmol/L). LCFA inhibited gastrin-stimulated gastric acid secretion by 4.1 mmol/15 min compared with 2.7 mmol/15 min for MCFA. PYY is therefore involved in the enterogastrone effect of MCFA; however, MCFA are less potent at inducing PYY release than LCFA. Greater induction of PYY release by LCFA may be due to CCK discharge by LCFA because CCK has been shown to stimulate PYY secretion. Other hormones may therefore be involved in the mechanism by which MCFA inhibit gastric acid secretion. However, except for GIP, which is not released in response to MCFA, these have not been studied.

Recently, Feinle et al. (29Citation ) investigated the ability of TG with fatty acids of varying chain lengths to induce gastrointestinal sensations and symptoms. Five different infusions were studied as follows: LCT (soybean oil), MCT, soy lecithin, Orlistat and sucrose polyester. LCT and MCT both increased gastric volume, with LCT causing the greater increase. All infusions resulted in increased feelings of fullness, bloating and nausea, and decreased hunger but effects were most pronounced with the LCT infusion. The authors concluded that the mechanism of action of fat in the generation of gastrointestinal symptoms required digestion of TG. Furthermore, because MCT do not release CCK, but do affect sensations of fullness, bloating and nausea, CCK-dependent and CCK-independent mechanisms must be involved.

In humans, MCFA do not stimulate CCK secretion. Therefore, CCK must not be the hormone responsible for their satiating effect (25Citation –29Citation ). Although MCT have been shown to induce satiety and to stimulate hormone secretion, no single hormone has been found to be strongly secreted due to MCT digestion. PYY has been found to be secreted in response to MCFA, yet it is still more potently secreted in response to LCT (27Citation ).


Potential Benefits to Consumption of MCT on Body Weight.
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There is evidence to suggest that short-term consumption of MCT increases EE in humans (3Citation –5Citation ,7Citation ,8Citation ) and results in decreased fat cell size and body weight accretion in animals (12Citation –16Citation ,19Citation ). Human studies have shown that replacing dietary LCT with MCT increases daily energy expenditure from 100 (6Citation ) to 669 kJ (7Citation ) in men and 138 kJ/d (8Citation ) in women. Studies examining the satiating effect of fats of different chain lengths found that energy intake was ~1070 kJ lower when meals contained MCT than when they contained LCT as the fat source (23Citation ). Van Wymelbeke et al. (24Citation ) found that intakes were 175–698 kJ lower, depending on the chain saturation of the LCT, at the subsequent meal when MCT were substituted for LCT. Therefore, in the most optimistic scenario in which EE would be increased by 669 kJ/d (7Citation ) and intakes decreased by 698 kJ/d (23Citation ), a weight gain of 1.35 kg/mo could be avoided by replacing LCT with MCT in the diet. On the other hand, the least optimistic scenario would give an increase in daily EE of 100 kJ (6Citation ) and decreased daily food intake of 350 kJ/d (2 subsequent meals, each less by 175 kJ) (24Citation ). In this case, a weight gain of 0.45 kg/mo would be avoided (Fig. 1Citation ). If we project these data to long-term weight balance, a negative weight balance of 5.4–16.2 kg/y would be produced. However, more work is required to establish whether prolonged consumption of MCT results in a decrease in BW or smaller weight gain compared with LCT.



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Figure 1. Replacement of dietary long-chain (LCT) for medium-chain triglycerides (MCT) can lead to increases in energy expenditure (EE) and satiety in humans. Energy expenditure can be increased by up to 460 kJ/d and food intake decreased by 175–698 kJ/d. The combination of increased energy expenditure and satiety can lead to prevention of body weight gain.


In summary, research conducted to date in animals shows that replacing dietary LCT by MCT causes a rise in EE, a depression of food intake and lower body fat mass. Similarly, in humans, MCT increase EE relative to LCT consumption. Fewer studies have examined the effects of MCT on satiety but, although results vary, these also suggest decreased food intake when LCT are replaced with MCT in the diet. Therefore, greater EE and lower food intake with MCT compared with LCT suggest that replacing dietary LCT with MCT could facilitate weight maintenance in humans.


FOOTNOTES

1 Manuscript received 16 October. Revision accepted 18 December 2001. Back

3 Abbreviations used: BW, body weight; CCK, cholecystokinin; CO, corn oil; DVZ, Devazepide; EE, energy expenditure; FO, fish oil; GIP, gastric inhibitory peptide; LCFA, long-chain fatty acids; LCT, long-chain triglycerides; MCFA, medium-chain fatty acids; MCT, medium-chain triglycerides; PYY, peptide YY; SCFA, short-chain fatty acids; SCT, short-chain triglycerides; TEF, thermic effect of food; TG, triglycerides. Back


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1. Babayan, V. K. (1987) Medium-chain triglycerides and structured lipids. Lipids 22:417-420.[Medline]

2. Bach, A. C. & Babayan, V. K. (1982) Medium-chain triglycerides: an update. Am. J. Clin. Nutr. 36:950-962.[Abstract]

3. Scalfi, L, Coltorti, A. & Contaldo, F. (1991) Postprandial thermogenesis in lean and obese subjects after meals supplemented with medium-chain and long-chain triglycerides. Am. J. Clin. Nutr. 53:1130-1133.[Abstract]

4. Seaton, T. B., Welle, S. L, Warenko, M. K. & Campbell, R. G. (1986) Thermic effect of medium-chain and long-chain triglycerides in man. Am. J. Clin. Nutr. 44:630-634.[Abstract]

5. Dulloo, A. G., Fathi, M., Mensi, N. & Girardier, L. (1996) Twenty-four-hour energy expenditure and urinary catecholamines of humans consuming low-to-moderate amounts of medium-chain triglycerides: a dose-response study in human respiratory chamber. Eur. J. Clin. Nutr. 50:152-158.[Medline]

6. Flatt, J. P., Ravussin, E., Acheson, K. J. & Jequier, E. (1985) Effects of dietary fat on postprandial substrate oxidation and on carbohydrate and fat balances. J. Clin. Investig. 76:1019-1024.[Medline]

7. Hill, J. O., Peters, J. C., Yang, D., Sharp, T., Kaler, M., Abumrad, N. N. & Greene, H. L. (1989) Thermogenesis in humans during overfeeding with medium-chain triglycerides. Metabolism 38:641-648.[Medline]

8. White, M. D., Papamandjaris, A. A. & Jones, P.J.H. (1999) Enhanced postprandial energy expenditure with medium-chain fatty acid feeding is attenuated after 14 d in premenopausal women. Am. J. Clin. Nutr. 69:883-889.[Abstract/Free Full Text]

9. Lasekan, J. B., Rivera, J., Hirvonen, M. D., Keesey, R. E. & Ney, D. M. (1992) Energy expenditure in rats maintained with intravenous or intragastric infusion of total parenteral nutrition solutions containing medium- or long-chain triglyceride emulsions. J. Nutr. 122:1483-1492.[Medline]

10. Mabayo, R. T., Furuse, M., Murai, A. & Okumura, J. I. (1994) Interactions between medium-chain and long-chain triacylglycerols in lipid and energy metabolism in growing chicks. Lipids 29:139-144.[Medline]

11. Rothwell, N. J. & Stock, M. J. (1987) Stimulation of thermogenesis and brown fat activity in rats fed medium chain triglyceride. Metabolism 36:128-130.[Medline]

12. Baba, N., Bracco, E. F. & Hashim, S. A. (1982) Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglyceride. Am. J. Clin. Nutr. 35:678-682.[Abstract]

13. Crozier, G., Bois-Joyeux, B., Chanez, M., Girard, J. & Peret, J. (1987) Metabolic effects induced by long-term feeding of medium-chain triglycerides in the rat. Metabolism 36:807-814.[Medline]

14. Geliebter, A., Torbay, N., Bracco, E., Hashim, S. A. & Van Itallie, T. B. (1983) Overfeeding with medium-chain triglyceride diet results in diminished deposition of fat. Am. J. Clin. Nutr. 37:1-4.[Abstract]

15. Lavau, M. M. & Hashim, S. A. (1978) Effect of medium chain triglyceride on lipogenesis and body fat in the rat. J. Nutr. 108:613-620.[Medline]

16. Hill, J. O., Peters, J. C., Lin, D., Yakubu, F., Greene, H. & Swift, L. (1993) Lipid accumulation and body fat distribution is influenced by type of dietary fat fed to rats. Int. J. Obes. 17:223-236.

17. Yost, T. J. & Eckel, R. H. (1989) Hypocaloric feeding in obese women: metabolic effects of medium-chain triglyceride substitution. Am. J. Clin. Nutr. 49:326-330.[Abstract]

18. St-Onge, M.-P., Bourque, C., Papamandjaris, A. A. & Jones, P.J.H. (2001) Consumption of medium chain triglycerides versus long chain triglycerides over 4 weeks increases energy expenditure and fat oxidation in obese women. Ann. Nutr. Metab. 45(suppl. 1):89(abs.).

19. Bray, G. A., Lee, M. & Bray, T. L. (1980) Weight gain of rats fed medium-chain triglycerides is less than rats fed long-chain triglycerides. Int. J. Obes. 4:27-32.[Medline]

20. Maggio, C. A. & Koopmans, H. S. (1982) Food intake after intragastric meals of short-, medium-, or long-chain triglyceride. Physiol. Behav. 28:921-926.[Medline]

21. Denbow, D. M., Van Krey, H. P., Lacy, M. P. & Watkins, B. A. (1992) The effect of triacylglycerol chain length on food intake in domestic fowl. Physiol. Behav. 51:1147-1150.[Medline]

22. Furuse, M., Choi, Y. H., Mabayo, R. T. & Okumura, J. I. (1992) Feeding behavior in rats fed diets containing medium chain triglyceride. Physiol. Behav. 52:815-817.[Medline]

23. Stubbs, R. J. & Harbron, C. G. (1996) Covert manipulation of the ration of medium- to long-chain triglycerides in isoenergetically dense diets: effect on food intake in ad libitum feeding men. Int. J. Obes. 20:435-444.

24. Van Wymelbeke, V., Himaya, A., Louis-Sylvestre, J. & Fantino, M. (1998) Influence of medium-chain and long-chain triacylglycerols on the control of food intake in men. Am. J. Clin. Nutr. 68:226-234.[Abstract]

25. McLaughlin, J., Luca, M. G., Jones, M. N., D’Amato, M., Dockray, G. J. & Thompson, D. G. (1999) Fatty acid chain length determines cholecystokinin secretion and effect on human gastric motility. Gastroenterology 116:46-53.[Medline]

26. Barbera, R., Peracchi, M., Cesana, B., Bianchi, P. A. & Basilisco, G. (2000) Sensations induce by medium and long chain triglycerides: role of gastric tone and hormones. Gut 46:32-36.[Abstract/Free Full Text]

27. Maas, M.I.M., Hopman, W.P.M., Katan, M. B. & Jansen, J.B.M.J. (1998) Release of peptide YY and inhibition of gastric acid secretion by long-chain and medium-chain triglycerides but not by sucrose polyester in men. Eur. J. Clin. Investig. 28:123-130.[Medline]

28. Maas, M.I.M., Hopman, W.P.M., Katan, M. B. & Jansen, J.B.M.J. (1996) Inhibition of gastrin-stimulated gastric acid secretion by medium-chain triglycerides and long-chain triglycerides in healthy young men. Regul. Pept. 66:203-210.[Medline]

29. Feinle, C., Rades, T., Otto, B. & Fried, M. (2001) Fat digestion modulated gastrointestinal sensations induced by gastric distension and duodenal lipid in humans. Gastroenterology 120:1100-1107.[Medline]

[DORIAN JR]

Another article "Physiological Effects of Medium-Chain Triglycerides: Potential Agents in the Prevention of Obesity" is another interesting one.

http://www.nutrition.org/cgi/content/full/132/3/329

Recent Advances in Nutritional Sciences
Physiological Effects of Medium-Chain Triglycerides: Potential Agents in the Prevention of Obesity1
Marie-Pierre St-Onge and Peter J. H. Jones2

School of Dietetics and Human Nutrition, McGill University, Ste-Anne-de-Bellevue, Quebec, Canada, H9X 3V9

2To whom correspondence should be addressed. E-mail: jonesp@macdonald.mcgill.ca.

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Medium chain fatty acids (MCFA) are readily oxidized in the liver. Animal and human studies have shown that the fast rate of oxidation of MCFA leads to greater energy expenditure (EE). Most animal studies have also demonstrated that the greater EE with MCFA relative to long-chain fatty acids (LCFA) results in less body weight gain and decreased size of fat depots after several months of consumption. Furthermore, both animal and human trials suggest a greater satiating effect of medium-chain triglycerides (MCT) compared with long-chain triglycerides (LCT). The aim of this review is to evaluate existing data describing the effects of MCT on EE and satiety and determine their potential efficacy as agents in the treatment of human obesity. Animal studies are summarized and human trials more systematically evaluated because the primary focus of this article is to examine the effects of MCT on human energy metabolism and satiety. Hormones including cholescytokinin, peptide YY, gastric inhibitory peptide, neurotensin and pancreatic polypeptide have been proposed to be involved in the mechanism by which MCT may induce satiety; however, the exact mechanisms have not been established. From the literature reviewed, we conclude that MCT increase energy expenditure, may result in faster satiety and facilitate weight control when included in the diet as a replacement for fats containing LCT.

KEY WORDS: • medium-chain triglycerides • satiety • energy expenditure • obesity


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Fats varying in fatty acid chain lengths are metabolized differently (1Citation –8Citation ). Medium-chain triglycerides (MCT),3 containing 6–12 carbon fatty acids, differ from long-chain triglycerides (LCT), which have fatty acids of > 12 carbons, in that they are absorbed directly into the portal circulation and transported to the liver for rapid oxidation (1Citation ). LCT, however, are transported via chylomicrons into the lymphatic system, allowing for extensive uptake into adipose tissue. Therefore, it has been hypothesized that the rapid metabolism of MCT may increase energy expenditure (EE), decrease their deposition into adipose tissue and result in faster satiety. The objective of the present article is to review literature concerning the effects of MCT on EE, fat deposition and food intake as a means to establish the potential efficacy of MCT in the prevention of obesity in humans.


Effect of MCT on Energy Expenditure.
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Animal trials studying the effects of MCT vs. LCT consumption on lipid and energy metabolism have shown that body weight (BW) is reduced with MCT consumption compared with LCT consumption and that feed efficiency is thus reduced (9Citation –11Citation ). In a study in which rats infused with MCT gained one third of the weight gained by those infused with LCT, Lasekan et al. (9Citation ) concluded that replacing LCT with MCT over long periods could produce weight loss without decreasing energy intakes.

Human studies have mainly compared the effects of MCT vs. LCT in single-meal or single-day experiments. Scalfi et al. (3Citation ) evaluated the effects of a single mixed meal containing MCT on postprandial thermogenesis and examined possible differences in the thermic response between lean and obese men. Subjects consumed a meal containing 15% of energy from protein, 55% from carbohydrate and 30% from fat, in the form of corn oil (CO) and animal fat or MCT oil (56% octanoate, 40% decanoate) in random order. Energy expenditure measurements were conducted before and for 6 h after consumption of the meal. Total EE was 48 and 65% greater in lean and obese individuals, respectively, after MCT compared with LCT consumption. Similar results were obtained by Seaton et al. (4Citation ) comparing the effects of MCT or CO on EE after a single meal. Energy expenditure peaked at 16% above baseline after MCT consumption compared with 5% for CO.

Dulloo et al. (5Citation ) investigated the thermogenic effects of low-to-moderate amounts of MCT consumption in healthy adult men. Subjects were required to spend 24 h in a respiratory chamber on four separate occasions; during that time, diets differed in the ratio of MCT:LCT (0:30, 5:25, 15:15, 30:0) provided as added fat. The diet was given at a level 1.4 times energy requirements and the 30 g of added fat was distributed evenly across all meals. The authors found that EE between 0800 and 2300 h increased by 45, 135 and 265 kJ with 5, 15 and 30 g of MCT in the diet, respectively. Mean 24-h EE also increased by 162 and 475 kJ with 15 and 30 g of MCT in added fat, respectively. Thus, the greater effects of MCT than LCT on EE are evident not only in the few hours after the meal but for a much longer time.

Most results (3Citation –5Citation ) from single-day experiments indicated that replacing LCT for MCT in the diet could produce weight loss after prolonged consumption. However, when Flatt et al. (6Citation ) compared diets rich in MCT, LCT and low in fat, they concluded that a low fat diet was more prudent when aiming for weight loss. However, MCT consumption resulted in greater EE at several time points compared with the low fat diet.

Few trials have been conducted over longer periods. One of those studies examined energy balance during the overfeeding of liquid formula diets containing MCT (61% octanoate, 32% decanoate) or LCT (32% oleate, 51% linoleate) for 7 d (7Citation ). EE was measured on d 1 and 6 for 10–15 min every 30 min for 6 h after meal consumption. The thermic effect of food (TEF) was identified as 8% of ingested energy after MCT consumption compared with 5.8% after LCT consumption on d 1. After 6 d, TEF was 12 and 6.6% of ingested energy with MCT and LCT consumption, respectively, indicating that the difference in EE between MCT and LCT persists even after a week of overfeeding.

The study of longest duration (14 d) published to date (8Citation ) sought to determine whether fatty acid chain length influenced EE and substrate oxidation in women. Subjects consumed a controlled, weight maintenance diet containing 40% of energy as fat, either in the form of butter and coconut oil (MCT; 38.9% of fatty acids contained chains with <16 carbons) or beef tallow. Energy expenditure was measured before and for 5.5 h after breakfast. Postprandial total EE after MCT consumption was greater than after LCT consumption on d 7 but not d 14. The authors concluded that the effects of MCT consumption on EE may be transient.

All animal studies (9Citation –11Citation ) and most human studies (3Citation –5Citation ,7Citation ,8Citation ) have shown that MCT consumption increases EE compared with a meal containing LCT. Investigators who found the greatest differences also concluded that MCT could be used in the treatment or prevention of human obesity (3Citation –5Citation ). However, the studies conducted to date have been short, ranging from a single meal (3Citation –6Citation ) to several days (7Citation ,8Citation ). Whether effects of MCT on EE and RQ are long lasting and result in actual measurable and sustainable changes in body composition of humans remain to be established.


Effect of MCT on Fat Deposition.
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Given that feed efficiency studies in animals and energetic studies in humans indicate enhanced EE after MCT consumption (3Citation –11Citation ), additional work has examined whether increased EE translates into decreased fat mass. In animals consuming MCT, BW were lower, fat depots smaller (12Citation –15Citation ) and adipocyte size smaller (12Citation ,13Citation ) with MCT compared with LCT consumption. These results led the authors to conclude that MCT could potentially prevent (13Citation ) or control (15Citation ) obesity in humans. However, MCT consumption was not observed by Hill et al. (16Citation ) to cause greater weight loss than lard, CO or fish oil (FO). Body adipose tissue during the first 3 mo was not different among groups but after 6 mo, the group fed FO had less body fat than all other groups. Although both FO and MCT feeding resulted in small fat cells, only FO feeding was associated with inhibition of cell proliferation.

Only one study evaluated the ability of MCT to facilitate weight reduction in humans (17Citation ). Obese women (n = 16) consumed MCT (58% octanoate, 22% decanoate) or LCT (soy oil) in random order for either 4 wk if they were inpatients or 12 wk if they were outpatients, at a level of 191 kJ/d. There were no differences in weight loss or rate of weight loss between diet treatments. A liquid diet containing 24% of energy as MCT failed to increase the rate of weight loss compared with LCT. This lack of agreement with animal trials and EE experiments may have been due to the low fat content of the diets (1.5 g of total fat/d, of which 1.2 g was treatment fat) or to gender differences in the effects of MCT. Differences detected in EE with MCT and LCT consumption are considerably greater in males than females. When data are extrapolated from trials conducted in men (3Citation –5Citation ,7Citation ), average EE was ~460 kJ/d greater with MCT than with LCT consumption, with a peak difference between treatments of 669 kJ/d (7Citation ). In contrast, data from White et al. (8Citation ), who studied women, found differences in EE of 138 kJ/d between MCT and LCT consumption. Our own work with overweight women also revealed a difference in EE of ~188 kJ/d (18Citation ). From these preliminary data, it appears that women respond less readily to treatment with MCT than men.


Effect of MCT on Food Intake and Satiety. Animal studies.
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Lower weight gain and decreased fat depot size with MCT feeding compared with LCT feeding in animals have been attributed to two different effects of MCT, i.e., increased EE and decreased food intake. Satiety may also be affected by fatty acid chain length of dietary fat. Bray et al. (19Citation ) observed greater feed intake when LCT were included in the diets of the rats compared with diets containing MCT. After 80 d of consuming diets containing 60% of energy from CO, MCT or a mixture of the two, rats fed the CO and the CO-MCT diets had a higher BW than those fed the MCT diet alone. Rats fed the MCT diet consumed less energy, and the authors concluded that ß-hydroxybutyrate may play a role in the difference in food intake between MCT- and CO-fed rats.

Given these results, Maggio and Koopmans (20Citation ), in 1982, conducted a study to clarify the origin and the nature of the signals that terminate short-term food intake of mixed meals containing triglycerides (TG) with fatty acids of different chain lengths. Sprague-Dawley rats were intubated intragastrically and given free access to a liquid diet containing 21% of energy as fat. The TG infusions consisted of 70% TG (tributyrin, tricaprylin or triolein in different concentrations) and 30% carbohydrate. Shifting chain length from medium to long did not differentially affect food intake when the infusions were equicaloric. Therefore, the authors concluded that satiety may be related to the amount of energy ingested rather than to the physical characteristics of the specific nutrients. This was in contrast to results obtained by Denbow et al. (21Citation ) who infused intrahepatically or intubated intragastrically white leghorn ****erels with isoenergetic quantities of tributyrate, tridecanoate or trioleate and measured feed consumption. Feed consumption with SCT and MCT infusion was suppressed within 1 h after intrahepatic infusion until 180 min. However, when infusions were given intragastrically, only SCT decreased feed intake. The authors concluded that these results reflect the relatively rapid rate of digestion and absorption of short-chain fatty acids (SCFA) from the gut along with oxidation of SCFA by the liver.

Furuse et al. (22Citation ) also investigated the effects of two different levels of MCT on feed intake in rats. They further examined the capacity of endogenous cholecystokinin (CCK) to modulate feed intake with MCT. Feed intake of male Wistar rats fed diets containing CO, MCT or a 1:1 mixture of CO and MCT was determined every hour for 12 h and then at 2-h intervals for the following 12 h. In a separate trial, Devazepide (DVZ), a CCK-A receptor antagonist, was injected intraperitoneally 40 min before feeding and feed intake was measured at 1, 2, 3 and 6 h postinjection. Feed intake decreased in a dose-dependent manner with increased concentration of MCT in the diet and was enhanced 2 h after DVZ injection. After 3 h, intake of the MCT diet was less than that of the CO diet. The authors thus concluded that satiety is affected by carbon chain length in dietary TG sources.


Effect of MCT on Food Intake and Satiety. Human studies.
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If MCT consumption enhances satiety and decreases food intake in animals, an equivalent response might be expected in humans. Stubbs and Harbron (23Citation ) examined whether the effects of ingesting MCT can limit the hyperphagia associated with high fat, energy-dense diets in humans. Six men participated in a three-phase inpatient trial in which they had free access to experimental high fat foods (61.5% of energy as fat) for 14 d. Each experimental phase differed in the amount of MCT included in the diet, i.e., low, medium or high MCT content with 20, 31 and 40%, respectively, of total energy as MCT. Subjects consumed 15.1 and 17.6 MJ less with the diet containing the most MCT compared with the diets containing the low and medium amounts of MCT, respectively, over the 14-d period. Body weights during consumption of the low and medium MCT diets increased by 0.45 and 0.41 kg, respectively, and decreased by 0.03 kg with the high MCT content diet. Food and energy intakes were thus suppressed when two thirds of the fat content of a high fat diet was derived from MCT, but BW were not affected.

Another clinical trial (24Citation ) was designed to establish the influence of chain length and degree of saturation on food intake in normal-weight men. Breakfasts differing in the nature of the fat, i.e., olive oil, lard, MCT or a fat substitute, were served and food intakes at lunch and dinner were measured. Energy intake at lunch was lower after the MCT-containing breakfast than after all other breakfasts (3100 vs. 3715 kJ with the fat substitute, 3278 kJ with olive oil and 3798 kJ with lard) but there were no differences in food consumption at dinner.


Hormones Iinvolved in the Satiating Effect of MCT and LCT.
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Clinical trials (23Citation ,24Citation ) have shown that MCT consumption can lead to lower energy intakes but have not explored the underlying mechanism. More recently, research has focused on specific hormones that may be involved in the satiating effect of MCT. McLaughlin et al. (25Citation ) examined the relationship among fatty acid chain length, CCK secretion, and proximal and distal gastric motor function. Healthy volunteers (n = 15) were studied for their response to a control meal and orogastric infusion of 250 mL of a 0.05 mol/L fatty acid emulsion. Fatty acid emulsions containing fatty acids of 11 carbon chains and less did not increase plasma CCK concentrations compared with the vehicle, whereas long-chain fatty acids (LCFA) did. This study showed that the human proximal gut differentiates between fatty acid molecules; however, it does not support the role of CCK in mediating the satiating effect of MCT.

Several other studies have also reported that MCT do not stimulate CCK secretion in humans (26Citation –28Citation ), and trials have attempted to establish which hormone is responsible for the observed effects of MCT on food intake. Barbera et al. (26Citation ) compared effects of MCT and LCT on sensations of satiety, gastric tone, gastric inhibitory peptide (GIP), pancreatic polypeptide and CCK. Subjects (n = 9) were infused with saline, LCFA (mainly oleate and linoleate) or MCFA (octanoate and decanoate) on three separate occasions in random order. LCFA infusion resulted in a greater rise in satiation than MCFA, but there was no difference between the two fats on the perception of fullness and bloating. The rise in gastric volume was also greater with LCFA infusion than MCFA infusion. Similarly, LCFA increased baseline levels of plasma CCK, GIP, neurotensin and pancreatic polypeptide compared with saline, whereas MCFA infusion did not. The authors thus concluded that MCFA induce gastric relaxation without increasing satiation or plasma levels of gut hormones. However, because Stubbs and Harbron (23Citation ) and Van Wymelbeke (24Citation ) have shown lower food intakes with diets rich in MCT, it is likely that other factors play a role in regulating energy balance with MCT consumption.

Maas et al. (27Citation ) examined effects of MCFA and LCFA on peptide YY (PYY) release to determine whether PYY, which inhibits gastric acid secretion in humans, is involved in the enterogastrone effect of MCFA. These investigators had previously observed that infusions of MCFA suppressed gastrin-stimulated gastric acid secretion without the involvement of CCK (28Citation ). Men (n = 14) were intraduodenally infused for 2.5 h with MCFA (56% octanoate, 43% decanoate), LCFA (CO) or saline in random order. The energy loads differed between MCFA and LCFA infusions, with the former providing a load of 11.6 kJ/min and the latter providing a load of 22.7 kJ/min. Both infusions increased plasma levels of PYY; however, LCFA resulted in a greater increase than MCFA infusion (10.3 vs. 2.8 pmol/L). LCFA inhibited gastrin-stimulated gastric acid secretion by 4.1 mmol/15 min compared with 2.7 mmol/15 min for MCFA. PYY is therefore involved in the enterogastrone effect of MCFA; however, MCFA are less potent at inducing PYY release than LCFA. Greater induction of PYY release by LCFA may be due to CCK discharge by LCFA because CCK has been shown to stimulate PYY secretion. Other hormones may therefore be involved in the mechanism by which MCFA inhibit gastric acid secretion. However, except for GIP, which is not released in response to MCFA, these have not been studied.

Recently, Feinle et al. (29Citation ) investigated the ability of TG with fatty acids of varying chain lengths to induce gastrointestinal sensations and symptoms. Five different infusions were studied as follows: LCT (soybean oil), MCT, soy lecithin, Orlistat and sucrose polyester. LCT and MCT both increased gastric volume, with LCT causing the greater increase. All infusions resulted in increased feelings of fullness, bloating and nausea, and decreased hunger but effects were most pronounced with the LCT infusion. The authors concluded that the mechanism of action of fat in the generation of gastrointestinal symptoms required digestion of TG. Furthermore, because MCT do not release CCK, but do affect sensations of fullness, bloating and nausea, CCK-dependent and CCK-independent mechanisms must be involved.

In humans, MCFA do not stimulate CCK secretion. Therefore, CCK must not be the hormone responsible for their satiating effect (25Citation –29Citation ). Although MCT have been shown to induce satiety and to stimulate hormone secretion, no single hormone has been found to be strongly secreted due to MCT digestion. PYY has been found to be secreted in response to MCFA, yet it is still more potently secreted in response to LCT (27Citation ).


Potential Benefits to Consumption of MCT on Body Weight.
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There is evidence to suggest that short-term consumption of MCT increases EE in humans (3Citation –5Citation ,7Citation ,8Citation ) and results in decreased fat cell size and body weight accretion in animals (12Citation –16Citation ,19Citation ). Human studies have shown that replacing dietary LCT with MCT increases daily energy expenditure from 100 (6Citation ) to 669 kJ (7Citation ) in men and 138 kJ/d (8Citation ) in women. Studies examining the satiating effect of fats of different chain lengths found that energy intake was ~1070 kJ lower when meals contained MCT than when they contained LCT as the fat source (23Citation ). Van Wymelbeke et al. (24Citation ) found that intakes were 175–698 kJ lower, depending on the chain saturation of the LCT, at the subsequent meal when MCT were substituted for LCT. Therefore, in the most optimistic scenario in which EE would be increased by 669 kJ/d (7Citation ) and intakes decreased by 698 kJ/d (23Citation ), a weight gain of 1.35 kg/mo could be avoided by replacing LCT with MCT in the diet. On the other hand, the least optimistic scenario would give an increase in daily EE of 100 kJ (6Citation ) and decreased daily food intake of 350 kJ/d (2 subsequent meals, each less by 175 kJ) (24Citation ). In this case, a weight gain of 0.45 kg/mo would be avoided (Fig. 1Citation ). If we project these data to long-term weight balance, a negative weight balance of 5.4–16.2 kg/y would be produced. However, more work is required to establish whether prolonged consumption of MCT results in a decrease in BW or smaller weight gain compared with LCT.



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Figure 1. Replacement of dietary long-chain (LCT) for medium-chain triglycerides (MCT) can lead to increases in energy expenditure (EE) and satiety in humans. Energy expenditure can be increased by up to 460 kJ/d and food intake decreased by 175–698 kJ/d. The combination of increased energy expenditure and satiety can lead to prevention of body weight gain.


In summary, research conducted to date in animals shows that replacing dietary LCT by MCT causes a rise in EE, a depression of food intake and lower body fat mass. Similarly, in humans, MCT increase EE relative to LCT consumption. Fewer studies have examined the effects of MCT on satiety but, although results vary, these also suggest decreased food intake when LCT are replaced with MCT in the diet. Therefore, greater EE and lower food intake with MCT compared with LCT suggest that replacing dietary LCT with MCT could facilitate weight maintenance in humans.


FOOTNOTES

1 Manuscript received 16 October. Revision accepted 18 December 2001. Back

3 Abbreviations used: BW, body weight; CCK, cholecystokinin; CO, corn oil; DVZ, Devazepide; EE, energy expenditure; FO, fish oil; GIP, gastric inhibitory peptide; LCFA, long-chain fatty acids; LCT, long-chain triglycerides; MCFA, medium-chain fatty acids; MCT, medium-chain triglycerides; PYY, peptide YY; SCFA, short-chain fatty acids; SCT, short-chain triglycerides; TEF, thermic effect of food; TG, triglycerides. Back


LITERATURE CITED
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1. Babayan, V. K. (1987) Medium-chain triglycerides and structured lipids. Lipids 22:417-420.[Medline]

2. Bach, A. C. & Babayan, V. K. (1982) Medium-chain triglycerides: an update. Am. J. Clin. Nutr. 36:950-962.[Abstract]

3. Scalfi, L, Coltorti, A. & Contaldo, F. (1991) Postprandial thermogenesis in lean and obese subjects after meals supplemented with medium-chain and long-chain triglycerides. Am. J. Clin. Nutr. 53:1130-1133.[Abstract]

4. Seaton, T. B., Welle, S. L, Warenko, M. K. & Campbell, R. G. (1986) Thermic effect of medium-chain and long-chain triglycerides in man. Am. J. Clin. Nutr. 44:630-634.[Abstract]

5. Dulloo, A. G., Fathi, M., Mensi, N. & Girardier, L. (1996) Twenty-four-hour energy expenditure and urinary catecholamines of humans consuming low-to-moderate amounts of medium-chain triglycerides: a dose-response study in human respiratory chamber. Eur. J. Clin. Nutr. 50:152-158.[Medline]

6. Flatt, J. P., Ravussin, E., Acheson, K. J. & Jequier, E. (1985) Effects of dietary fat on postprandial substrate oxidation and on carbohydrate and fat balances. J. Clin. Investig. 76:1019-1024.[Medline]

7. Hill, J. O., Peters, J. C., Yang, D., Sharp, T., Kaler, M., Abumrad, N. N. & Greene, H. L. (1989) Thermogenesis in humans during overfeeding with medium-chain triglycerides. Metabolism 38:641-648.[Medline]

8. White, M. D., Papamandjaris, A. A. & Jones, P.J.H. (1999) Enhanced postprandial energy expenditure with medium-chain fatty acid feeding is attenuated after 14 d in premenopausal women. Am. J. Clin. Nutr. 69:883-889.[Abstract/Free Full Text]

9. Lasekan, J. B., Rivera, J., Hirvonen, M. D., Keesey, R. E. & Ney, D. M. (1992) Energy expenditure in rats maintained with intravenous or intragastric infusion of total parenteral nutrition solutions containing medium- or long-chain triglyceride emulsions. J. Nutr. 122:1483-1492.[Medline]

10. Mabayo, R. T., Furuse, M., Murai, A. & Okumura, J. I. (1994) Interactions between medium-chain and long-chain triacylglycerols in lipid and energy metabolism in growing chicks. Lipids 29:139-144.[Medline]

11. Rothwell, N. J. & Stock, M. J. (1987) Stimulation of thermogenesis and brown fat activity in rats fed medium chain triglyceride. Metabolism 36:128-130.[Medline]

12. Baba, N., Bracco, E. F. & Hashim, S. A. (1982) Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglyceride. Am. J. Clin. Nutr. 35:678-682.[Abstract]

13. Crozier, G., Bois-Joyeux, B., Chanez, M., Girard, J. & Peret, J. (1987) Metabolic effects induced by long-term feeding of medium-chain triglycerides in the rat. Metabolism 36:807-814.[Medline]

14. Geliebter, A., Torbay, N., Bracco, E., Hashim, S. A. & Van Itallie, T. B. (1983) Overfeeding with medium-chain triglyceride diet results in diminished deposition of fat. Am. J. Clin. Nutr. 37:1-4.[Abstract]

15. Lavau, M. M. & Hashim, S. A. (1978) Effect of medium chain triglyceride on lipogenesis and body fat in the rat. J. Nutr. 108:613-620.[Medline]

16. Hill, J. O., Peters, J. C., Lin, D., Yakubu, F., Greene, H. & Swift, L. (1993) Lipid accumulation and body fat distribution is influenced by type of dietary fat fed to rats. Int. J. Obes. 17:223-236.

17. Yost, T. J. & Eckel, R. H. (1989) Hypocaloric feeding in obese women: metabolic effects of medium-chain triglyceride substitution. Am. J. Clin. Nutr. 49:326-330.[Abstract]

18. St-Onge, M.-P., Bourque, C., Papamandjaris, A. A. & Jones, P.J.H. (2001) Consumption of medium chain triglycerides versus long chain triglycerides over 4 weeks increases energy expenditure and fat oxidation in obese women. Ann. Nutr. Metab. 45(suppl. 1):89(abs.).

19. Bray, G. A., Lee, M. & Bray, T. L. (1980) Weight gain of rats fed medium-chain triglycerides is less than rats fed long-chain triglycerides. Int. J. Obes. 4:27-32.[Medline]

20. Maggio, C. A. & Koopmans, H. S. (1982) Food intake after intragastric meals of short-, medium-, or long-chain triglyceride. Physiol. Behav. 28:921-926.[Medline]

21. Denbow, D. M., Van Krey, H. P., Lacy, M. P. & Watkins, B. A. (1992) The effect of triacylglycerol chain length on food intake in domestic fowl. Physiol. Behav. 51:1147-1150.[Medline]

22. Furuse, M., Choi, Y. H., Mabayo, R. T. & Okumura, J. I. (1992) Feeding behavior in rats fed diets containing medium chain triglyceride. Physiol. Behav. 52:815-817.[Medline]

23. Stubbs, R. J. & Harbron, C. G. (1996) Covert manipulation of the ration of medium- to long-chain triglycerides in isoenergetically dense diets: effect on food intake in ad libitum feeding men. Int. J. Obes. 20:435-444.

24. Van Wymelbeke, V., Himaya, A., Louis-Sylvestre, J. & Fantino, M. (1998) Influence of medium-chain and long-chain triacylglycerols on the control of food intake in men. Am. J. Clin. Nutr. 68:226-234.[Abstract]

25. McLaughlin, J., Luca, M. G., Jones, M. N., D’Amato, M., Dockray, G. J. & Thompson, D. G. (1999) Fatty acid chain length determines cholecystokinin secretion and effect on human gastric motility. Gastroenterology 116:46-53.[Medline]

26. Barbera, R., Peracchi, M., Cesana, B., Bianchi, P. A. & Basilisco, G. (2000) Sensations induce by medium and long chain triglycerides: role of gastric tone and hormones. Gut 46:32-36.[Abstract/Free Full Text]

27. Maas, M.I.M., Hopman, W.P.M., Katan, M. B. & Jansen, J.B.M.J. (1998) Release of peptide YY and inhibition of gastric acid secretion by long-chain and medium-chain triglycerides but not by sucrose polyester in men. Eur. J. Clin. Investig. 28:123-130.[Medline]

28. Maas, M.I.M., Hopman, W.P.M., Katan, M. B. & Jansen, J.B.M.J. (1996) Inhibition of gastrin-stimulated gastric acid secretion by medium-chain triglycerides and long-chain triglycerides in healthy young men. Regul. Pept. 66:203-210.[Medline]

29. Feinle, C., Rades, T., Otto, B. & Fried, M. (2001) Fat digestion modulated gastrointestinal sensations induced by gastric distension and duodenal lipid in humans. Gastroenterology 120:1100-1107.[Medline]

Post Extras: Print Post Remind Me! Notify Moderator

[TM40]

What is the optimal time to supplement with the different EFAs? With the research on MCT and coconut oil it would seem that the best times for supplementation might be before exercise (both cardio and weight lifting). Flax oil after meal 4 or so (of 7 or 8) and before bed. I still take coconut oil and flax on a cut, not only on a bulk, because of the health benefits. What do you think?

TM

[Venom]

Both are excellent fats; so almost any time would be great. I would agree thta MCT oil would see to be a good choice pre-exercise. Many prefer to have their EFA's in their post workout meal; since it is known to enhance insulin sensitivity, this would be rather logical. Otherwise, I always have one or the other with my low carb meals to help spare protein.

And my fat is typically higher on my cuts than bulks. So yes, use them whether your goal is to loose or gain weight.

[TM40]

Thanks Venom.

[W8isGR8]

I didn't get a chance to read the whole thread yet, so excuse me if this question has already been asked.


I know everyone is against fat intake directly post-workout, but wouldn't taking in MCT's ensure that the carbs/protein be used for glycogen and protein synthesis. I'm sure these are energy-costly events, so intaking MCT's would keep the body from using some of the protein/carbs as fuel.

[newbuilder]

Venom,

That article looks dense! Perhaps I will find the time to understand it!

[Venom]

newbuilder,

I hope so, too. /forum/images/graemlins/grin.gif Let us know if you have any questions. /forum/images/graemlins/smile.gif

W8isGR8,

Welcome to ABC /forum/images/graemlins/laugh.gif

[ QUOTE ]

I know everyone is against fat intake directly post-workout, but wouldn't taking in MCT's ensure that the carbs/protein be used for glycogen and protein synthesis. I'm sure these are energy-costly events, so intaking MCT's would keep the body from using some of the protein/carbs as fuel.

[/ QUOTE ]

First, I think it is great that you are thinking critcally. /forum/images/graemlins/cool.gif

Some problems would be that:

1. It would slow digestion
2. You don't need fat post workout
3. You should never combine high fat meals and spike insulin. Insulin blunts fat oxidation; thus, you increase the chance of storing that fat--even though it is MCT oil--as adipose tissue.

[newbuilder]

[ QUOTE ]
newbuilder,

I hope so, too. Let us know if you have any questions.

W8isGR8,

Welcome to ABC

[/ QUOTE ]

Right On!
I could spend all night on this article! I have just made a one hour study out of it.
Thanks!

As is stated in the beginning of the article - bodybuilding is taking the nutrients that God graciously gives us, and we give our bodies, and using them for anablic purposes and away from fat storing purposes.
If saturated fats have a single bond and are then more stable - does this then mean that they are less susceptible to oxidation?
Since unsaturated fats are less stable, does this mean that oxidation occurs more readily?
OK. That means if it is oxidized,it is burned or used for energy, or for an anabolic reaction. I am straight with that.
It just seems to me that the whole biochemical process of the body metabolism and muscle building is so complex and at the same time is much like feeding or even just making a fire - with fuel, oxygen, heat from exercise, chemical reactions and chain reactions - and then regulation the the heat and the processes for optimal gains the end.
So are new muscle tissue then the biproduct of a chemical reaction within the body?
In this process there must be something else that is created -heat? or gas?
So the question I have to be solved is what is the equation?
This plus this plus this equals new muscle, with the byproduct of this and this.
Does saturated or unsaturated fat fit into this or play an integral part in the process of forming a new muscle cell?

These are some ideas I have come up with from what I have studied here.
Hope this helps! I am here to serve you too!

[W8isGR8]

[ QUOTE ]
Some problems would be that:

1. It would slow digestion
2. You don't need fat post workout
3. You should never combine high fat meals and spike insulin. Insulin blunts fat oxidation; thus, you increase the chance of storing that fat--even though it is MCT oil--as adipose tissue.

[/ QUOTE ]
I still feel pretty strongly that the benifits would outweigh any consequence.

1. MCT's digest differently than regular fats, much quicker since they bypass the normal pathways of fat digestion. So saying they would slow down digestion is like saying that sticking your hand out the window would slow down your car on the freeway /forum/images/graemlins/tongue.gif After all, whey and dextrose/malto are some of the quickest digesting foods around.

2. You're right, you need energy. Energy to synthesize protein, replenish glygogen, restore ATP, etc. Why rob the proein/carbs from your PWO shake when you could supply your body with a prefered fuel source?

I figure that after the thermic effect of digestion(metabolic cost), as well as the energy cost of all the gowth/repairs your body needs, over half your PWO meal is gone. That only leaves you with half the materials for muscle building.

[Venom]

[ QUOTE ]

1. MCT's digest differently than regular fats, much quicker since they bypass the normal pathways of fat digestion. So saying they would slow down digestion is like saying that sticking your hand out the window would slow down your car on the freeway After all, whey and dextrose/malto are some of the quickest digesting foods around.

[/ QUOTE ]

I think that is a bit exaggerated. /forum/images/graemlins/wink.gif


[ QUOTE ]

2. You're right, you need energy. Energy to synthesize protein, replenish glygogen, restore ATP, etc. Why rob the proein/carbs from your PWO shake when you could supply your body with a prefered fuel source?

[/ QUOTE ]

I don't understand what you are saying here? Are you saying MCT oil is a preferred energy source over carbs?


[ QUOTE ]

I figure that after the thermic effect of digestion(metabolic cost), as well as the energy cost of all the gowth/repairs your body needs, over half your PWO meal is gone. That only leaves you with half the materials for muscle building.

[/ QUOTE ]

If this is the case, there are two possible ways to handle this:

1. Increase your post workout shake by upping your carbs and proteins
2. Have another meal 1 hour after.

So why have fat when you could just up protein and carbs?