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  1. #1
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    Medscape Article about ALA
    Alpha-lipoic acid decreases thiol reactivity of the insulin receptor and protein tyrosine phosphatase 1B in 3T3-L1 adipocytes.
    Biochem Pharmacol 2003 Sep 1;66(5):849-58 (ISSN: 0006-2952)
    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.

  2. #2
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    can you please put that in laymens terms doc i understand some of it but midway through -- well i am lost -- lol

  3. #3
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    The last line is the conclusion. Oxidants produced by either ALA or insulin activate the insulin receptor and deactivate protein tyrosine phosphatases, which results in increased glucose uptake in adipose tissue. This article supports someone's conclusion that ALA can make one fatter. I take no sides in the ongoing debate. I prefer metformin.

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    thank you doc

  5. #5
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    Originally posted by DrJMW
    The last line is the conclusion. Oxidants produced by either ALA or insulin activate the insulin receptor and deactivate protein tyrosine phosphatases, which results in increased glucose uptake in adipose tissue. This article supports someone's conclusion that ALA can make one fatter. I take no sides in the ongoing debate. I prefer metformin.
    Excellent post doc.......def sets the stage again for a hell of argument!

  6. #6
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    not really. the uptake of GLYCOGEN into adipose tissue is not a bad thing. their other study, on which this one is based, shows inhibition of differentitation and fatty acid synthesis. the PPAR-y issue.


    as a note the average person can store 15g of glycogen/1kg of mass. with 10-20% of that being stored in muscle tissue.

  7. #7
    I am banned! Drveejay11's Avatar
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    Originally posted by DrJMW
    I prefer metformin.
    WHY glucophage over Avandia? Is there evidence that the increased insulin sensitivity caused by Glucophage's/Metformin's ability to inhibit hepatic glucose production and increasing the sensitivity of peripheral tissues to insulin is advantageous to Avandia's ability to sensitize the cells to insulin more effectively (and NOT just in the periphery?

    How can we be sure (here we go again ) that Glucophage will drive the nutrients favorably into the skeletal muscles vs the adipocytes?

  8. #8
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    As I pointed out when Animal posted this same study, the author Lester Packer, who is the world's foremost authority on Lipoic Acid does not endorse the use of ALA over R+ ALA. He has written and lectured many times about the superiority of R+ over racemate.


    "R[+]-LA [that is, R(+)-lipoic acid], and not a racemic mixture of R[+]-and S[-]- LA, should be considered a choice for therapeutic applications."
    Dr. Lester Packer and colleagues, in Free Radical Biology and Medicine.

    Who is Dr Packer?

    Dr. Lester Packer, the world's foremost antioxidant research scientist, received his Ph.D. in Microbiology and Biochemistry from Yale University and has been a Professor and Senior Researcher at the University of California at Berkeley for the past 40 years. Most recently, Dr. Packer has established an additional research laboratory in the Dept. of Molecular Pharmacology & Toxicology within the School of Pharmacy at the University of Southern California to pursue studies related to the molecular, cellular, and physiological aspects of free radical and antioxidant metabolisms in biological systems.

    In addition to his membership in more than a dozen professional research societies, Dr. Packer has held offices as President of the International Society of Free Radical Research, President of the Oxygen Club of California, and Vice-President of UNESCO - the United Nations Global Network on Molecular and Cell Biology.

    Dr. Packer is also the recipient of numerous scientific achievement awards and serves on editorial advisory boards for scientific journals related to biochemistry, antioxidant metabolism and nutrition.

    Dr. Packer has published over 700 scientific papers and 70 books on every aspect of antioxidants and health, including the standard references "Vitamin E in Health and Disease", "Vitamin C in Health and Disease", "The Handbook of Natural Antioxidants" and "Understanding the Process of Aging:The Roles of Mitochondria, Free Radicals, and Antioxidants".


    In other words, this guy knows his shite. I have spoken with him and will be joining Macro in Calif for a one on one conference with him as a consultant to Glucorell R. And now I am posting more than I should be.
    Last edited by ulter; 02-05-2004 at 06:38 PM.

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    LOLOL...animal where art thou

  10. #10
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    Post by drveejay


    The last line is the conclusion. Oxidants produced by either ALA or insulin activate the insulin receptor and deactivate protein tyrosine phosphatases, which results in increased glucose uptake in adipose tissue. This article supports someone's conclusion that ALA can make one fatter. I take no sides in the ongoing debate. I prefer metformin.'



    AAAAAAAAAAAAAAAAAAAAAAAAAAAAHHAHAHAHAHAHAHAHAHAHAH AHAHAHAHAHAHAHA!


    HAAAAAAAAAAAA!

    And then somebody says glucose uptake into fat cells isn't bad.

    SINCE WHEN?

    Like I've been saying all along! At least now you see how the story is changing NOT that it doesn't do EXACTLY what I said it does, but now that what THEY say it does isn't bad?

    Please post the info and studies where it's good for us to jam sugar into our fat cells.

    And I'll be, if ALA is jamming glucose AND AA's in there, THAT'S even worse as the fat cells are sucking up AA's my muscle wants.

    OOOOOOOOOOOOOUUUUUUUUUUUUCH!

    Who gives a rats ass about what a doctor does or doesn't do in his little world. Lectures are nice.

    Nevertheless, I didn't say r didn't work for it's ORIGINAL intended method, but I did SAY that it's BAD for the intended bill of goods you are being sold!

    Now why is it good for glucose to go into my fat cells and AA's, too? I'm stupid so fill this board with the studies.

    TTRRRRRRRRRRRRUUUUUUUUUUMP!

    It sucks to be RRRRRRRRRRIIIIIIIIIIIIGHT!

  11. #11
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    your inability to understand even the basic mechanisms of human physiology are astounding.

    why dont you explain again why it is that you want fat cells to be insulin resistant? because diabetes is such a wonderful condition.
    btw- in case you had not figured it out insulin resistant fat cells=diabetes.

    and as you have failed to understand it, glucose uptake is but part of r+ lipoics actions. Your failure to look at the system as opposed to a single facet is why you are unable to comprehend.

    and you again make an erroneous conclusion, lipoic acid has no impact on amino acid uptake, in either fat or muscle cells. do you just make this stuff up?

  12. #12
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    Originally posted by Animalkits


    Who gives a rats ass about what a doctor does or doesn't do in his little world. Lectures are nice.

    less than 24 hours ago you were referring to DR AMES, who is the Second most authority on R+, as the end all be all.

    weird logic. or perhaps just self serving logic

  13. #13
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    well bro's....personally i jumped on the r-ala bandwagon, and i thought i was seeing decent results. however the results could have benn attributed to my training, aas, and the fact i run growth about 6-8 months a year......so

    well i am going to stop taking the R-ala for a month and see if i notice anything different. i understand the doctors theory, and have to admit, it supports Animals case. there is one way to find out, i'll give myself my own R-ALA test...and i'll let you guys know how it turns out.

    god bless

  14. #14
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    WE are NOT diabetics, but this is your BEST argument!

    HAHA!

    'R+ Lipoic Acid is a prescription treatment for diabetes in Germany and other European countries. The reason is that it lowers insulin levels and causes greater glucose uptake..'

    Please post all the pictures of lean and mean diabetics as well as showing it causes fat loss.

    YOU CANNOT.

    You also CANNOT compare insulin insensitivity in DIABETICS with normal humans and athletes! YOU do not even know that it's better to have glucose ANYWHERE in a diabetic except in the bloodstream? There's a reason diabetes is called 'sugar' and extended sugar in the blood in DIABETICS causes major problems so ANY means is used to get it out including increasing insulin and using ALA to dump it into the FAT CELLS!

    But please, feel free to call me uneducated while you dupe people into believing they are diabetics in need of glucose clearance into their fat cells.

    Where is the study that such is good for you and reduces fat mass? HAHA!

  15. #15
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    "You also CANNOT compare insulin insensitivity in DIABETICS with normal humans and athletes! "

    This is probably true but you're leaving out the fact that all this changes as you become insulin resistant (like those diabetics) when you take Anabolic Steroids. Which is why we concentrate the sales of Glucorell R to people over 40 and people who use steroids, you know, like on these boards. It also helps those who are overweight and have a history of poor eating habits since these people can become insulin resistant and develope adult onset diabetes as early as age 11. See cover of Time Magazine December 8, 2003.

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    That's ok with me if that's how you represent it!

    People who take H, and insulin, and use some kinds of AS could be resistant as they made themselves that way. At such a point of course it would be better to have glucose going into fat cells over having it in the bloodstream.

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    The problem I have seen with Avandia is that clients were getting fat. I have not seen any fat gain with Glucophage. Now, studies are looking at combined glucophage/avandia therapy. While glucophage does sensitize the insulin receptor a little, its main function is to prevent gluconeogenesis in the liver. Avandia, on the other hand, its main function is to sensitize insulin receptors. Unfortunately, it is non-selective. It also sensitizes insulin receptors in adipose tissue. Glucophage, on the other hand--all of the studies I have seen, no one has gained fat.

  18. #18
    I am banned! Drveejay11's Avatar
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    Originally posted by DrJMW
    The problem I have seen with Avandia is that clients were getting fat. I have not seen any fat gain with Glucophage. Now, studies are looking at combined glucophage/avandia therapy. While glucophage does sensitize the insulin receptor a little, its main function is to prevent gluconeogenesis in the liver. Avandia, on the other hand, its main function is to sensitize insulin receptors. Unfortunately, it is non-selective. It also sensitizes insulin receptors in adipose tissue. Glucophage, on the other hand--all of the studies I have seen, no one has gained fat.
    Interesting. Thanks

  19. #19
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    Originally posted by macro
    less than 24 hours ago you were referring to DR AMES, who is the Second most authority on R+, as the end all be all.

    weird logic. or perhaps just self serving logic
    What a signifcant point of discussion! Please fill the threads with more posts as such as well as showing I ever referred to him at any time.

    More changing the subject to make it about ME.

    Thanks, bud and if you dilute the thread, maybe the sheep will forget the facts!

  20. #20
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    Originally posted by DrJMW
    The problem I have seen with Avandia is that clients were getting fat. I have not seen any fat gain with Glucophage. Now, studies are looking at combined glucophage/avandia therapy. While glucophage does sensitize the insulin receptor a little, its main function is to prevent gluconeogenesis in the liver. Avandia, on the other hand, its main function is to sensitize insulin receptors. Unfortunately, it is non-selective. It also sensitizes insulin receptors in adipose tissue. Glucophage, on the other hand--all of the studies I have seen, no one has gained fat.
    OUCH!

    And isn't the claim to ALA the same?

    Ooops.

    We have one chemical making people fat as it sensitizes fat cells while another chemical donig the EXACT same thing somehow magically doesn't get the same results.

  21. #21
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    Originally posted by Animalkits
    What a signifcant point of discussion! Please fill the threads with more posts as such as well as showing I ever referred to him at any time.

    More changing the subject to make it about ME.

    Thanks, bud and if you dilute the thread, maybe the sheep will forget the facts!
    Originally posted by Animalkits


    A real published doctor actually came up with the ALA with ALC and maybe you should read it one day where you can learn what it really does for normal people.
    he's the author of this study.

  22. #22
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    A slight increase of glucose uptake into adipocytes can be beneficial because it simulates leptin synthesis and release.. Leptin is involved in the regulation of energy homeostasis, an increase of leptin can increase thermogenesis and ********* rate, decrease food intake,decrease insulin mediated lipogenesis,etc...

    ALA decreases adipogenesis induced by insulin , the net result of ALA administration is decreased fat mass which was actually shown in vivo, in normal nondiabetic rats:


    http://jap.physiology.org/cgi/content/full/92/1/50

    ..."An important observation in the present study is that chronic treatment of lean animals with R-ALA was associated with a significantly reduced rate of body weight gain (Table 1). As lean mass was apparently not affected (muscle wet weights were not different between sedentary and R-ALA-treated animals), the difference in body mass was likely due to a difference in fat mass. It has previously been noted that, in older rats, chronic treatment with R-ALA leads to increases in ambulatory activity and hepatocellular oxygen consumption (8), and we have also found increases in ********* enzyme activities (hexokinase and citrate synthase; Figs. 5 and 6) in skeletal muscle of the R-ALA-treated animals. The possibility exists that chronic R-ALA treatment can increase the expression of specific genes involved in metabolism, allowing for an increase in ********* and ambulatory activity and ultimately leading to a reduced body weight gain..."

  23. #23
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    Ahhhhhh........it was only a matter of time before my boy HAJ broke out the knowledge..........NOW it gets GOOD!

    Nice Post.

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    Of course some others will tell you that if you work out you are insulin resistant!

    'IT IS WELL ESTABLISHED that endurance exercise training leads to an enhancement of insulin-mediated glucose metabolism (see reviews in Refs. 11, 15, 16). In normal rodent models, moderate- or high-intensity exercise training can improve glucose tolerance (2, 20), whole body insulin sensitivity (21, 22), and insulin action on skeletal muscle glucose transport activity in rodent models (13, 30, 34). The increased insulin action on skeletal muscle glucose transport after exercise training is associated with increased GLUT-4 protein expression (7, 13, 25, 30, 31, 34) as well as with adaptive responses of enzymes involved in glucose phosphorylation and oxidation (15, 16).'

    (I know EXACTLY what I'm talking about)

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    And the beat all end all!

    Insulin is NOT REDUCED!

    Plasma glucose, insulin, and free fatty acids. There were no differences in plasma glucose among the various groups after the overnight food restriction (Table 1). R-ALA treatment had no effect on plasma levels of insulin, whereas exercise training induced significant decreases in plasma insulin (23-33%) and free fatty acids (62-136%) compared with all other groups. In contrast, R-ALA treatment resulted in the highest level of circulating free fatty acids, an effect that was prevented by exercise training of R-ALA-treated animals.

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