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Role of hyperglucagonemia in maintenance of increased rates of hepatic glucose output in type II diabetics

Below is a hypothetical scenario to demonstrate my point: An individual suffers from long-term thiamine deficiency and has suboptimal riboflavin status Thiamine deficiency leads to lower activity of transketolase Low transketolase activity produces a lack of NADPH A lack of NADPH and a lack of FAD means that glutathione reductase is unable to efficiently recycle glutathione, which produces an imbalance between reduced/oxidized glutathione

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