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This intestine-centered reprogramming of systemic glucose flux mirrors metabolic changes observed in other therapeutic contexts, such as bariatric surgery [73], suggesting that the intestine may function as an active regulator of glucose disposal rather than solely as an absorptive barrier, and given that the intestine represents a primary site of metformin action, these alterations in intestinal glucose flux been increasingly recognized as an important component in elucidating the mechanism of action of metformin

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1 Heart-rate changes can persist longer but tend to plateau or decline as treatment continues