Insulin resistance in SM is the primary defect of T2DM that facilitates the progression of fatty liver disease, deposition of fat in the liver (Figure 1) (110)
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As MOTS-c activates AMPK and NRF2, it also indirectly suppresses the mTOR (mechanistic target of rapamycin) pathway, the master growth and anabolism regulator that, when chronically overactivated, accelerates the accumulation of senescent cells
