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Abbreviations: * indicates significant change; FDR, first degree relatives of patients with type 2 diabetes; FG, fasting glucose; FI, fasting insulin; MCR, metabolic clearance rate of glucose; NC, no change; PCO, women with polycystic ovary syndrome; ~ indicates values taken from a figure.

Abbreviations: * indicates significant change; FDR, first degree relatives of patients with type 2 diabetes; FG, fasting glucose; FI, fasting insulin; MCR, metabolic clearance rate of glucose; NC, no change; PCO, women with polycystic ovary syndrome; ~ indicates values taken from a figure.

reduction in body weight per se reduces insulin resistance this may also represent a mechanism by which metformin improves insulin resistance.

To summarize, the partly divergent observations from the numerous metabolic studies regarding metformin's effect on muscle and liver (Fig. 4 and 5) may reflect different mechanisms of metformin action in the basal versus the insulin-stimulated state. In the basal, postabsorptive state the improvement of fasting hyperglycemia is mostly due to a decrease of the accelerated endogenous glucose production. This results from inhibition of both gluconeogenesis and glycogen breakdown. Direct or indirect effects on regulatory enzymes are likely to be involved. No data are available for suppression of glucose production during experimental hyperinsulinemia. However, the fact that reduction in basal glucose production occurs in the presence of lower or unaltered insulin levels suggests that glucose production in liver and kidney (66,67) is more sensitive to the restrictive action of insulin after treatment with metformin.

In the insulin-stimulated state during the clamp peripheral glucose disposal is increased even in the absence of improved fasting glycemia indicating a reduction in insulin resistance. This is thought to be mainly a result of enhanced glucose transport and storage in muscle. The effect on glucose transport is most likely due to a potentiation of insulin-stimulated translocation of glucose transporters and an increase in their intrinsic activity (68,69). Glycogen synthesis is increased as a result of stimulatory effects of metformin on the signaling chain to activation of glycogen synthase. Moreover, the in vivo effect on muscle may in part be due to a reduction in FFA oxidation. Finally, in insulin-resistant subjects the effect on muscle appears to be more pronounced suggesting a reversal of insulin resistance rather than a mere improvement in insulin sensitivity.

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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