Research Question of the Week: How to Optimize Fat Efficiency in the Diet - Page 6 - ABCbodybuilding

Go Back   ABCbodybuilding > Scientist Department > HYPERplasia Research

Notices

Reply
 
Thread Tools
  #51  
Old 01-12-2006, 09:43 PM
Venom's Avatar
Venom Venom is offline
Venom is training, researching, or talking on ABC
Vice President Abcbodybuilding.com
 
Join Date: Apr 2001
Location: The Pain Zone
Posts: 19,500
Default Re: Research Question of the Week: How to Optimize Fat Efficiency in the Diet

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!
__________________
Gabriel "Venom" Wilson, Ph.D. Nutritional Sciences
B.S. (Hons) & M.S. in Kinesiology, CSCS
Vice President, ABCbodybuilding
Co-Editor. of JHR

Venom@abcbodybuilding.com
Bible Studies
Click Here to Support the Future of Bodybuilding!


Matthew 7:20
And Jesus said unto them, Because of your unbelief: for verily I say unto you, If ye have faith as a grain of mustard seed, ye shall say unto this mountain, Remove hence to yonder place; and it shall remove; and nothing shall be impossible unto you.
Reply With Quote
  #52  
Old 01-13-2006, 02:01 PM
ryancostill ryancostill is offline
ryancostill should change his/her status!
Super-Heavyweight
 
Join Date: Apr 2003
Posts: 4,886
Default Re: Research Question of the Week: How to Optimize Fat Efficiency in the Diet

[ 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.
__________________
The virtue of all achievement is victory over oneself. Those who know this can never know defeat.

http://www.london2012.com/NR/rdonlyr...ghtlifting.jpg

Creatine: A literature review

Creatine: Practical Applications

International Symposium of Biomechanics in Sport
Reply With Quote
  #53  
Old 01-13-2006, 07:12 PM
Damien Voorhees's Avatar
Damien Voorhees Damien Voorhees is offline
Damien Voorhees should change his/her status!
Lightweight
 
Join Date: May 2005
Posts: 440
Default Re: Research Question of the Week: How to Optimize Fat Efficiency in the Diet

There is gelato everywhere in Italy but perhaps that's their only vice! Well, of course, there is the wine! [img]/forum/images/graemlins/smile.gif[/img]
Reply With Quote
  #54  
Old 01-18-2006, 10:08 PM
ryancostill ryancostill is offline
ryancostill should change his/her status!
Super-Heavyweight
 
Join Date: Apr 2003
Posts: 4,886
Default Re: Research Question of the Week: How to Optimize Fat Efficiency in the Diet

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?
__________________
The virtue of all achievement is victory over oneself. Those who know this can never know defeat.

http://www.london2012.com/NR/rdonlyr...ghtlifting.jpg

Creatine: A literature review

Creatine: Practical Applications

International Symposium of Biomechanics in Sport
Reply With Quote
  #55  
Old 01-18-2006, 10:50 PM
sucramdw sucramdw is offline
sucramdw should change his/her status!
Super-Heavyweight
 
Join Date: Jul 2004
Location: San Diego
Posts: 3,837
Default Re: Research Question of the Week: How to Optimize Fat Efficiency in the Diet

[ 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%.
Reply With Quote
  #56  
Old 01-19-2006, 08:42 AM
ryancostill ryancostill is offline
ryancostill should change his/her status!
Super-Heavyweight
 
Join Date: Apr 2003
Posts: 4,886
Default Re: Research Question of the Week: How to Optimize Fat Efficiency in the Diet

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.
__________________
The virtue of all achievement is victory over oneself. Those who know this can never know defeat.

http://www.london2012.com/NR/rdonlyr...ghtlifting.jpg

Creatine: A literature review

Creatine: Practical Applications

International Symposium of Biomechanics in Sport
Reply With Quote
  #57  
Old 02-24-2006, 04:07 AM
**DONOTDELETE**
**DONOTDELETE** should change his/her status! Edit
Guest
 
Posts: n/a
Default Re: Research Question of the Week: How to Optimize Fat Efficiency in the Diet

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 ί-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 ί-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.

ί-hydroxybutyrate plasma levels. ί-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 ΅g 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
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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%).


View this table:
[in this window]
[in a new window]
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.



View larger version (39K):
[in this window]
[in a new window]
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).



View larger version (25K):
[in this window]
[in a new window]
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.


ί-hydroxybutyrate plasma levels. The ί-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 ί-hydroxybutyrate plasma concentration in rats fed MF-MCT was intermediate between its concentration in rats fed LF-MCT and LF-safflower (Fig. 3).



View larger version (31K):
[in this window]
[in a new window]
Figure 3. Plasma ί-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
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
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 ί-hydroxybutyrate was also significantly higher in rats fed LF-MCT compared with rats fed LF-safflower in this study, whereas ί-hydroxybutyrate plasma concentration of rats fed MF-MCT was intermediate. This parallel pattern of ί-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
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES


1. Carriere F, Barrowman JA, Verger R, Laugier R 1993 Secretion and contribution to lipolysis of gastric and pancreatic lowpass during a test meal in humans. Gastroenterology 105: 876–888[Medline]
2. Payne RM, Sims HF, Jennens ML, Lowe ME 1994 Rat pancreatic lipase and two related proteins: enzymatic properties and mRNA expression during development. Am J Physiol 266: G914–G921[Medline]
3. Brannon PM 1990 Adaptation of the exocrine pancreas to diet. Ann Rev Nutr 10: 85–105[CrossRef][Medline]
4. Dagorn JC 1986 Mechanism of pancreas adaptation to diet. Biochimie 68: 329–331
5. Gidez LI 1973 Effect of dietary fat on pancreatic lipase levels in the rat. J Lipid Res 14: 169–177[Medline]
6. Lowe ME, Rosenblum JL, Strauss AW 1989 Cloning and characterization of human pancreatic lipase cDNA. J Biol Chem 264: 20042–20048[Abstract/Free Full Text]
7. Wicker-Planquart C, Puigserver A 1992 Primary structure of rat pancreatic lipase mRNA. FEBS Lett 296: 61–66[CrossRef][Medline]
8. Giller T, Buchwald P, Blum-Kaelin D, Hunziker W 1992 Two novel human pancreatic lipase related proteins, hPLRP1 and hPLRP2. J Biol Chem 267: 16509–16516[Abstract/Free Full Text]
9. Crenon I, Jayne S, Kerfelec B, Hermoso J, Pignol D, Chapus C 1998 Pancreatic lipase-related protein type 1: a double mutation restores a significant lipase activity. Biochem Biophys Res Commun 246: 513–517[CrossRef][Medline]
10. Lowe ME 1997 Molecular mechanisms of rat and human pancreatic triglyceride lipase. J Nutr 127: 549–557[Abstract/Free Full Text]
11. Andersson L, Carriere F, Lowe ME, Nilson A, Verger R 1996 Pancreatic lipase-related protein 2 but not classical pancreatic lipase hydrolyzes galactolipids. Biochim Biophys Acta 1302: 236–240[Medline]
12. Spannagel AW, Nakano I, Tawil T, Chey WY, Liddle RA, Green GM 1996 Adaptation to fat markedly increases pancreatic secretory response to intraduodenal fat in rats. Am J Physiol 270: G128–G135[Medline]
13. Schwizer W, Asal K, Kreiss C, Mettraux C, Borovicka J, Remy R, Guezelhan C, Hartman D, Fried M 1997 Role of lipase in the regulation of upper gastrointestinal function in humans. Am J Physiol 273: G612–G620[Medline]
14. Wicker C, Puigserver A 1989 Changes in mRNA levels of rat pancreatic lipase in the early days of consumption of a high lipid diet. Eur J Biochem 180: 563–567[Abstract]
15. Wicker C, Puigserver A 1990 Expression of rat pancreatic lipase gene is modulated by a lipid-rich diet at a transcriptional level. Biochem Biophy Res Commun 166: 358–364[Medline]
16. Ricketts J, Brannon PM 1994 Amount and type of dietary fat regulate pancreatic lipase gene expression in rats. J Nutr 124: 1166–1171[Medline]
17. Deschodt-Lanckman M, Robberecht P, Camus J, Christophe J 1971 Short- term adaptation of pancreatic lipase hydrolases to nutritional and physiological stimuli in adult rats. Biochemie 53: 789–796[Medline]
18. Saraux B, Girard-Globa A, Ouagued M, Vacher D 1982 Response of the exocrine pancreas to quantitative and qualitative variations in dietary lipids. Am J Physiol 243: G10–G15[Medline]
19. Sabb JE, Godfrey PM, Brannon PM 1986 Adaptive response of rat pancreatic lipase to dietary fat: effects of amount and type of fat. J Nutr 116: 892–899[Medline]
20. Hamosh M 1995 Lipid metabolism in pediatric nutrition. Pediatric Clin N Am 42: 839–859
21. Bach AC, Igenbleek Y, Frey A 1996 The usefulness of dietary medium chain triglycerides in body weight control: fact or fantasy? J Lipid Res 37: 708–726[Abstract]
22. Bach AC, Babayan VK 1982 Medium chain triglycerides: an update. Am J Clin Nutr 36: 950–962[Abstract]
23. Schneeman BO, Gallaher D 1980 Changes in small intestinal digestive enzyme activity and bile acids with dietary cellulose in rats. J Nutr 110: 584–590[Medline]
24. Lowry OH, Rosenbaugh NJ, Farr AL, Randell RJ 1951 Protein measurement with the folin phenol reagent. J Biol Chem 193: 265–275[Free Full Text]
25. Williamson DH, Mellanby J, Krebs HA 1962 Enzymatic determination of D (-) ί-hydroxybutyric acid and acetoacetic acid in blood. Biochem J 82: 90–96
26. Chomczynski P, Sacchi N 1987 Single step method of isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. Anal Biochem 162: 156–159[CrossRef][Medline]
27. Steinhilber W, Poensgen J, Rausch U, Kern HF, Scheele GA 1988 Translational control of anionic trypsinogen and amylase synthesis in rat pancreas in response to caerulein stimulation. Proc Natl Acad Sci U S A 85: 6597–6601[Abstract]
28. Wishart MJ, Andrews PC, Nichols R, Blevis GT, Logsdon CD, Williams JA 1993 Identification and cloning of the GP-3 from rat pancreatic acinar zymogen granules as a glycosylated membrane-associated lipase. J Biol Chem 268: 10303–10311[Abstract/Free Full Text]
29. Grusby MJ, Nabavi N, Wong H, Dick RF, Bluestone JA, Schotz MC, Glimcher LH 1990 Cloning of an interleukin-4 inducible gene from cytotoxic T lymphocytes and its identification as a lipase. Cell 60: 451–459[CrossRef][Medline]
30. Tsai A, Cowan MR, Johnson DG, Brannon PM 1994 Regulation of pancreatic amylase and lipase gene expression by diet and insulin in diabetic rats. Am J Physiol 267: G575–583[Medline]
31. Steel RGD, Torrie JH 1960 Principles and Procedures of Statistics. McGraw-Hill, New York
32. Tantibhedhyangkul P, Hashim SA 1975 Medium-chain triglyceride feeding in premature infants: effect on fat and nitrogen absorption. Pediatrics 55: 359–365[Abstract]
33. Odle J 1997 New insights into the utilization of medium chain triglycerides by the neonate; observations from a piglet model. J Nutr 127: 1061–1067[Abstract/Free Full Text]
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
37. Duan R, Erlanson-Albertsson C 1992 Gastric inhibitory polypeptide stimulates pancreatic lipase and colipase synthesis in rats. Am J Physiol 262: G779–G784[Medline]
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]
39. Benzonana G, Desnuelle P 1968 Action of some effectors on the hydrolysis of long-chain triglycerides by pancreatic lipase. Biochim Biophys Acta 164: 47–58[Medline]
40. Lien EL 1994 The role of fatty acid composition and positional distribution in fat absorption in infants. J Pediatr 125: s62–s68[Medline]
41. Hashim SA, Tantibhedyangkul P 1987 Medium chain triglyceride in early life: effects on growth on growth of adipose tissue. Lipids 22: 429–434[Medline]
42. Tantibhedhyangkul P, Hashim SA 1978 Medium-chain triglyceride feeding in premature infants: effect on calcium and magnesium absorption. Pediatrics 61: 537–545[Abstract]
43. Hamosh M, Mehta NR, Fink CS, Coleman J, Hamosh P 1991 Fat absorption in premature infants: medium chain triglycerides and long chain triglycerides are absorbed from formula at similar rates. J Pediatr Gastroenterol Nutr 28: 143–149[CrossRef]
44. Sulkers HJ, vGoudoever JB, Leunisse C, Wattimena JLD, Sauer PJJ 1992 Comparison of two preterm formulas with or without addition of medium-chain triglycerides (MCTs). I: Effect on nitrogen and fat balance and body composition changes. J Pediatr Gastroenterol Nutr 15: 34–41[Medline]
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.
Reply With Quote
  #58  
Old 02-24-2006, 04:14 AM
**DONOTDELETE**
**DONOTDELETE** should change his/her status! Edit
Guest
 
Posts: n/a
Default Re: Research Question of the Week: How to Optimize Fat Efficiency in the Diet

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.

Back


ABSTRACT
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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


INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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.
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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.
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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.
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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 ί-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.
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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.
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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.
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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.



View larger version (18K):
[in this window]
[in a new window]
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
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED


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]
Reply With Quote
  #59  
Old 02-24-2006, 04:16 AM
DORIAN JR's Avatar
DORIAN JR DORIAN JR is offline
DORIAN JR should change his/her status!
Bantamweight
 
Join Date: Jan 2006
Location: Temple Gym
Posts: 228
Default Re: Research Question of the Week: How to Optimize Fat Efficiency in the Diet

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.

Back


ABSTRACT
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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


INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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.
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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.
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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.
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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 ί-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.
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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.
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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.
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED

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.



View larger version (18K):
[in this window]
[in a new window]
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
TOP
ABSTRACT
INTRODUCTION
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Effect of MCT on...
Hormones Iinvolved in the...
Potential Benefits to...
LITERATURE CITED


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
Reply With Quote
  #60  
Old 02-27-2006, 04:53 PM
TM40 TM40 is offline
TM40 should change his/her status!
Newbie
 
Join Date: May 2005
Location: MI
Posts: 88
Default Re: Research Question of the Week: How to Optimize Fat Efficiency in the Diet

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
__________________
I Like Toast.
Reply With Quote
Reply

Thread Tools

Posting Rules
You may not post new threads
You may not post replies
You may not post attachments
You may not edit your posts

BB code is On
Smilies are On
[IMG] code is On
HTML code is Off
Forum Jump


All times are GMT. The time now is 11:38 AM.


Powered by vBulletin® Version 3.7.2
Copyright ©2000 - 2014, Jelsoft Enterprises Ltd.