Milos Sarcev's take on ALA & insulin

[DougoeFre5h]

http://www.milossarcev.com/cgi-bin/y...num=1076868208

"I started looking into available research and I’ve found some studies that compared ALA to insulin . While it was evident that ALA is glucose-lowering agent it appeared that ALA’s regulation of glucose metabolism in the muscle is quite different than insulin’s. Insulin clearly produced dramatic enhancement in glycogen synthesis and the same was expected from ALA. What was discovered was surprising. It seemed that ALA actually acted as inhibitor of glycogen synthesis and caused considerable glucose oxidation! Of course, experiences of several of my guinea pigs from Gold’s Gym of Fullerton is not
enough to publish a study in New England Journal of Medicine, but their results were confirming that what’s found in some animal studies could be true for humans as well. I still recommend modest doses of alpha lipoic acid daily (400mg after the breakfast) for its ability to eliminate free radicals and enhance our immune system with the increase of intracellular glutathione. Also, I would like to mention that ALA is valuable hepatoprotector frequently used for the treatment of liver diseases. However, exact time when ALA should not be used is - in the post workout drink! To conclude, this is only my personal opinion (and opinion of half of the members of the Gold’s Gym in Fullerton…)"

I haven't put much effort into researching this, but as Milos sees it, ALA should NOT be taken post w/o. Is he correct in his assumptions?

[einstein1905]

No, I disagree with him. First off, studies show that r-ALA autophosphorylates the insulin receptor, which increases glucose uptake (the study I'm posting used adipocytes, but the insulin receptor is the same in muscle). My little experiment showed a marked drop in BG post workout. Even if ALA causes glucose uptake and then glucose oxidation, that provides intracellular "energy" to drive pwo protein synthesis. When we say "replenish muscle glycogen stores", we don't mean that so literally. We are providing intracellular glucose to first drive the immediate required pwo protein synthesis that occurs, as the rebuilding process begins. Glycogen is simply glucose polymers and must be broken down into glucose to be usable. So, we provide glucose to drive immediate requirements, and excess contributes to glycogenesis.


Biochem Pharmacol. 2003 Sep 1;66(5):849-58. Related Articles, Links


Alpha-lipoic acid decreases thiol reactivity of the insulin receptor and protein tyrosine phosphatase 1B in 3T3-L1 adipocytes.

Cho KJ, Moini H, Shon HK, Chung AS, Packer L.

Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-171, South Korea.

Alpha-lipoic acid is known to increase insulin sensitivity in vivo and to stimulate glucose uptake into adipose and muscle cells in vitro. In this study, alpha-lipoic acid was demonstrated to stimulate the autophosphorylation of insulin receptor and glucose uptake into 3T3-L1 adipocytes by reducing the thiol reactivity of intracellular proteins. To elucidate mechanism of this effect, role of protein thiol groups and H(2)O(2) in insulin receptor autophosphorylation and glucose uptake was investigated in 3T3-L1 adipocytes following stimulation with alpha-lipoic acid. Alpha-lipoic acid or insulin treatment of adipocytes increased intracellular level of oxidants, decreased thiol reactivity of the insulin receptor beta-subunit, increased tyrosine phosphorylation of the insulin receptor, and enhanced glucose uptake. Alpha-lipoic acid or insulin-stimulated glucose uptake was inhibited (i) by alkylation of intracellular, but not extracellular, thiol groups downstream of insulin receptor activation, and (ii) by diphenylene iodonium at the level of the insulin receptor autophosphorylation. alpha-Lipoic acid also inhibited protein tyrosine phosphatase activity and decreased thiol reactivity of protein tyrosine phosphatase 1B. These findings indicate that oxidants produced by alpha-lipoic acid or insulin are involved in activation of insulin receptor and in inactivation of protein tyrosine phosphatases, which eventually result in elevated glucose uptake into 3T3-L1 adipocytes.

[flexshack]

which eventually result in elevated glucose uptake into 3T3-L1 adipocytes.

einstein, wouldn't this be considered a bad effect of ala?

[einstein1905]

einstein, wouldn't this be considered a bad effect of ala?

It's a trade off, as is the case with insulin itself. That's why pwo dietary intake is crucial....limiting fats being primary....controlling carb intake being nearly as important.