Glut 4 is activated by what compound?

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    Glut 4 is activated by what compound?


    anyone that knows...I'm looking for the specific ingredient ..not anabolic pump , or Yellow Gold.

    Mullet you keep talking about Glut 4 in your posts . do you know?
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    Corosolic acid I believe
    Muscle Pharm Rep
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    Why isnt it listed in the anabolic pump ingredients?

    P-Insulin (Engineered Extract from Phellodendron)

    Tannins Complex (Engineered Extract from Lagerstroemia Speciosa)


    I havnt researched all the Yellow Gold's many different compounds; however there main Berberine-containing plants, berberine has shown not to stimulate glut 4, and is questionable about stimulating glut 1; although it may.
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    Berberine stimulates GLUT4 translocation, unless you can show me a study which says otherwise (I admittedly have not been keeping up with my research). Specifically, Corosolic Acid, and more likely the Tannins in Lagerstroemia (Tannic Acid) stimulate GLUT4 translocation.
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    I found my first article saying bererines increased GLUT4 translocation in L6 cells in a phosphatidylinositol 3' kinase–independent manner, and reduced lipid accumulation in 3T3-L1 adipocytes.

    I wonder which one is older and newer research

    http://diabetes.diabetesjournals.org...urcetype=HWCIT
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    Two of the articles above are the same, as an FYI.

    AMPk is immediately involved in the glycogen uptake pathway via induction of GLUT4; especially in terms of contractile tissue. GLUT4 mRNA expression and translocation can be adversely affected by the downregulation of AMPk and other kinases. Without methods and materials (i.e. the full-texts of those articles) we don't know whether simply the translocation of GLUT4 was not noted, or whether mRNA expression was not noted. Further, the second study you cited did not speak to GLUT4, but merely AMPk, which as shown above directly mediates GLUT4.
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    On the Pubmed study

    "But berberine affected the expression of GLUT4 neither in normal nor in insulin-resistant cells."

    In other words Berberine didn't effect Glut 4 in normal or in insulin-resistant cells.
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    Quote Originally Posted by smeton_yea View Post
    On the Pubmed study

    "But berberine affected the expression of GLUT4 neither in normal nor in insulin-resistant cells."

    In other words Berberine didn't effect Glut 4 in normal or in insulin-resistant cells.
    Please see above.

    AMPk is immediately involved in the glycogen uptake pathway via induction of GLUT4; especially in terms of contractile tissue. GLUT4 mRNA expression and translocation can be adversely affected by the downregulation of AMPk and other kinases. Without methods and materials (i.e. the full-texts of those articles) we don't know whether simply the translocation of GLUT4 was not noted, or whether mRNA expression was not noted. Further, the second study you cited did not speak to GLUT4, but merely AMPk, which as shown above directly mediates GLUT4.
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    Berberine-stimulated glucose uptake in L6 myotubes involves both AMPK and p38 MAPK

    Zhe Cheng, Tao Pang, Min Gu, An-Hui Gao, Chuan-Ming Xie, Jing-Ya Li, Fa-Jun Nan and Jia Li

    National Center for Drug Screening, Shanghai Institute of Materia Medica, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 201203, P. R. China


    Received 17 May 2006; revised 13 September 2006; accepted 13 September 2006. Available online 20 September 2006.

    Abstract

    Berberine is a plant alkaloid used in traditional Chinese medicine and has been reported to have antihyperglycemic activity in NIDDM patients. However, the molecular basis for this action is yet to be elucidated. Here we investigate the effects and signaling pathways of berberine on L6 rat skeletal muscles. Our study demonstrates that berberine stimulates glucose uptake in a time- and dose-dependent manner. Intriguingly, berberine-stimulated glucose uptake does not vary as insulin concentration increases, and could not be blocked by the PI 3-kinase inhibitor wortmannin. Berberine only weakly stimulates the phosphorylation of Akt/PKB, a key molecule in the insulin signaling pathway, but strongly promotes the phosphorylation of AMPK and p38 MAPK. The effects of berberine are not a result of pro-oxidant action, but a consequence of an increased cellular AMP:ATP ratio. Moreover, berberine-stimulated glucose uptake is inhibited by the AMPK inhibitor Compound C and the p38 MAPK inhibitor SB202190. Inhibition of AMPK reduces p38 MAPK phosphorylation, suggesting that AMPK lies upstream of p38 MAPK. These results suggest that berberine circumvents insulin signaling pathways and stimulates glucose uptake through the AMP-AMPK-p38 MAPK pathway, which may account for the antihyperglycemic effects of this drug.
  

  
 

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