Although senescence of hepatic cells (e.g., hepatocytes and hepatic stellate cells, mainly driven by mitochondrial dysfunction, altered lipid metabolism, liver fat accumulation), adipose tissue (dysfunctional cells, increased inflammation, decreased insulin sensitivity and lipid storage) and muscle cells (mainly by through increased oxidative cells and mitochondrial dysfunction) may contribute to T2D development, cellular senescence of pancreatic β-cells is emerging as one major determinant for T2D etiopathogenesis [62,84,85]. Here, INS is linked to type 2 diabetes mellitus.