Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance, the hallmark of type 2 diabetes mellitus T2DM. However, the cause-effect relationship remains to be fully elucidated. Compelling evidence suggests that boosting mitochondrial function may represent a valuable therapeutic tool to improve insulin sensitivity. However, these processes appear to be dysregulated in type 2 diabetic individuals. Herein, we describe the mechanistic link between mitochondrial dysfunction and insulin resistance in skeletal muscle alongside the intracellular pathways orchestrating mitochondrial bioenergetics. We then review current evidence on nutritional tools, including fatty acids, amino acids, caloric restriction and food bioactive derivatives, which may enhance insulin sensitivity by therapeutically targeting mitochondrial function and biogenesis. Obesity has reached epidemic proportions worldwide and its incidence is on the rise affecting both adults and children 1. Of note, obesity and visceral fat accumulation in particular are underlain by a low-grade chronic inflammation Hotamisligil, and increased ectopic fat storage in metabolically active tissues including skeletal muscle and liver, a phenomenon termed lipotoxicity Unger,
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