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Diabetic and corticosteroid-impaired models are used to characterize these mechanisms under conditions of disrupted tissue repair

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In mouse models of insulin resistance, it significantly inhibits NNMT activity in liver and muscle, reduces NAM methylation, increases intracellular NAD+, activates the SIRT1 pathway, promotes phosphorylation of insulin receptor substrate 1 (IRS1), enhances insulin signaling, improves insulin sensitivity, and increases glucose uptake and utilization

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