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Blinding of AMP-dependent kinase by methylglyoxal: A mechanism that allows perpetuation of hepatic insulin resistance
Medical Hypotheses, 08/13/09
Gugliucci A – The authors hypothesize that excess MG in the above–mentioned conditions blocks the sensing of AMP by AMPK, thereby favoring gluconeogenesis (thus hepatic glucose output and hyperglycemia) and lipogenesis (hepatic steatosis and high VLDL), hallmarks of insulin resistance and diabetes. The hypothesis may explain, for instance, the perpetuation of hepatic insulin resistance, as well as part of the action of metformin, which is a potent anti–glycation agent.
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