Diet for obese vs. lean individuals - insulin sensitivity - Page 3 - ABCbodybuilding

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  #21  
Old 05-14-2009, 09:31 PM
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YOU ARE KIDDING ME!!! I am in a rush, so can't respond much, but that is awesome research, Jer!!

J Appl Physiol 106: 1425-1434, 2009


The antioxidant {alpha}-lipoic acid (LA) has been shown to improve insulin action in high-fat (HF)-fed animal models, yet little is known about its underlying mechanisms of action. We hypothesize that LA acts by inducing heat shock proteins (HSPs), which then inhibit stress kinases known to interfere with insulin signaling intermediates. Male Wistar rats were fed a HF diet (60% calories from fat) for 6 wk, while controls received a chow diet (10% calories from fat). One-half of the rats in each group received daily LA injections (30 mg/kg body wt). In rats fed a HF diet, LA increased expression of HSP72 and activation of HSP25 in soleus muscle, but it had no effect on HSPs in muscle from chow-fed rats. LA treatment reduced phosphorylation of c-Jun NH2-terminal kinase (JNK) and inhibitor of {kappa}B kinase-β (IKKβ) activity (I{kappa}B{alpha} protein levels) in rats fed a HF diet and effectively restored insulin responsiveness, as seen by insulin-stimulated phosphorylated Akt/Akt and 2-deoxyglucose uptake in soleus muscle. LA also induced activation of p38 MAPK and AMP-activated protein kinase, proteins previously implicated in insulin-independent glucose uptake. In addition, acute LA treatment induced HSPs in vitro in L6 muscle cells and prevented the activation of JNK and IKKβ with stimulants such as anisomycin and TNF-{alpha}, respectively. In conclusion, our results suggest chronic LA treatment results in stress kinase inhibition and improved insulin signaling through a HSP-mediated mechanism.
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  #22  
Old 05-15-2009, 02:30 AM
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Thanks for the feedback Ben - much valued.

I definitely like the insulin sensitizing agents like ALA and cinnamon. These agents are actually most potent in these pops where oxidative stress and metabolic abnormalities are so high. So totally agree with that.

Pretty excited about this idea...I think we may be on to something here. This is why I love science!!
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Last edited by Venom; 05-15-2009 at 02:33 AM.
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  #23  
Old 05-15-2009, 05:08 PM
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J Appl Physiol 106: 1425-1434, 2009


The antioxidant {alpha}-lipoic acid (LA) has been shown to improve insulin action in high-fat (HF)-fed animal models, yet little is known about its underlying mechanisms of action. We hypothesize that LA acts by inducing heat shock proteins (HSPs), which then inhibit stress kinases known to interfere with insulin signaling intermediates. Male Wistar rats were fed a HF diet (60% calories from fat) for 6 wk, while controls received a chow diet (10% calories from fat). One-half of the rats in each group received daily LA injections (30 mg/kg body wt). In rats fed a HF diet, LA increased expression of HSP72 and activation of HSP25 in soleus muscle, but it had no effect on HSPs in muscle from chow-fed rats. LA treatment reduced phosphorylation of c-Jun NH2-terminal kinase (JNK) and inhibitor of {kappa}B kinase-β (IKKβ) activity (I{kappa}B{alpha} protein levels) in rats fed a HF diet and effectively restored insulin responsiveness, as seen by insulin-stimulated phosphorylated Akt/Akt and 2-deoxyglucose uptake in soleus muscle. LA also induced activation of p38 MAPK and AMP-activated protein kinase, proteins previously implicated in insulin-independent glucose uptake. In addition, acute LA treatment induced HSPs in vitro in L6 muscle cells and prevented the activation of JNK and IKKβ with stimulants such as anisomycin and TNF-{alpha}, respectively. In conclusion, our results suggest chronic LA treatment results in stress kinase inhibition and improved insulin signaling through a HSP-mediated mechanism.
****! Crazy stuff, thanks jer
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Old 05-15-2009, 05:13 PM
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Originally Posted by Venom View Post
Thanks for the feedback Ben - much valued.

I definitely like the insulin sensitizing agents like ALA and cinnamon. These agents are actually most potent in these pops where oxidative stress and metabolic abnormalities are so high. So totally agree with that.

Pretty excited about this idea...I think we may be on to something here. This is why I love science!!
My pleasure..
Exactly Gabe!
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Old 05-16-2009, 11:20 PM
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Just from personal experience I find that I am much more sensitive to carbs when I am leaner (< 10 %) than in my upper range of bodyfat (12 %).

I agree with you Gabe. One of the things I really want to write about on abc is insulin, insulin resistance, bulking etc. Literally break this subject down like we have done for protein. This has been on my mind for years now. And I think we have the scientific prowess on our site to team up and get this job done.
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Old 05-16-2009, 11:22 PM
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Thanks for those insight Jer and Ben! You guys kick behind.

I am going to take my ALA now :-P
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Old 05-22-2009, 10:04 PM
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Just from personal experience I find that I am much more sensitive to carbs when I am leaner (< 10 %) than in my upper range of bodyfat (12 %).

I agree with you Gabe. One of the things I really want to write about on abc is insulin, insulin resistance, bulking etc. Literally break this subject down like we have done for protein. This has been on my mind for years now. And I think we have the scientific prowess on our site to team up and get this job done.
I am certainly in for that challenge!

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Thanks for those insight Jer and Ben! You guys kick behind.

I am going to take my ALA now :-P
No prob! hah ALA is the bomb
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  #28  
Old 06-02-2009, 10:56 PM
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In that line of thought, J. I think if you train your body right, then all you need are minor adjustments. For example, if you make your body very sensitive to insulin, leptin, etc. Then you don't need to bump your carbs from 100 to 600! All you need is to bump them a little and you'll get the maximal response. In fact, that is the definition of insulin sensitivity - the amount of insulin required to get half the maximal response. If you require less, you are more sensitive.
but venom, isn't going over caloric maintenance still the fundamental rule you must follow in order to gain muscle? and if you are very insulin sensitive, then techincally you will secrete LESS insulin per meal, so you have less of that anabolic hormone, and overtime less insulin = less igf-1, which is something I read elsewhere saying insulin and igf-1 directly related.

for being lean all of it seems to make sense, less insulin more of the other hormone (was it glucagon?) but for gaining I think we run into the problem of not having enough calories and potentially stifling the insulin response. I think that's why bottom line odds are no matter how clean you bulk you will still get fat?
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  #29  
Old 06-03-2009, 12:36 AM
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Absolutely, being in a caloric surplus is important for getting huge. This post was centered on people cutting, though.

About insulin sensitivity, more insulin does not = more effective response from insulin. Obese get constant supplies of insulin in the blood. But studies show they are actually less anabolic, and don't stimulate muscle protein synthesis as potently in response to a meal as lean people. Why? One reason is because they are insensitive to anabolic factors like insulin.

The point of insulin sensitivity, is that you require less insulin to get a maximal response - so with half the amount of insulin, a lean person can dispose of the same amount of glucose as an overweight person (just threw out a general number there). Same thing applies for anabolic factors like IGF.

So insulin sensitivity is a good thing...
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  #30  
Old 06-03-2009, 12:50 PM
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this interests me, a question. if someone is obese they are carrying alot of fat so their maintence calories for the muscle mass they hold is lower than total calores they would need to stay same weight, does this mean obese people fall into a half and half catagory where they can when dieting, get a surplus of calories high enough to build muscle mass but lower than their 'total' weight maintence calorie needs and losefat at the same time?
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