INS and familial primary hypomagnesemia: At the molecular level, it has been suggested that hypomagnesemia may induce altered cellular glucose transport, defective tyrosine-kinase activity, and insulin receptor autophosphorylation, post-receptor impairment in insulin action by influencing intracellular signaling cascade and processing, reduced pancreatic insulin secretion, and worsening of insulin resistance in diabetics [37,38,39,40].