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This leads to an increase in both glucose-dependent synthesis of insulin and in vivo secretion of insulin from pancreatic beta-cells, by mechanisms involving cyclic AMP and/or other intracellular signaling pathways

This oxidization contributes considerably to the T2D pathology, possibly by activating alternative downstream signaling pathways critically involved in insulin resistance and compromised insulin secretion [10]

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This has led to a focus on signaling pathways and neuroendocrine mechanisms to develop targeted obesity treatments

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