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This progressive deficit leads to insufficient sirtuin activation, mitochondrial respiratory chain dysfunction, and decreased ATP production (Rajman et al., Cell Metab 2018)

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for MetS and T2D), and because exercise is one of the most potent IGF-1 synthesis/freeing mechanisms, it seems logical to correlate them and establish IGF-1 as a target for future options in the multifactorial treatment for metabolic syndrome

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