Magnesium (in its ionized and biologically active form, Mg2+) is an essential trace element that participates in numerous physiologic processes. Abnormal Mg2+ homeostasis can lead to many metabolic disorders, including diabetes mellitus (DM) and its complications. Mg2+ participates in energy generation and is required for DNA and RNA synthesis, reproduction, and protein synthesis. Additionally, Mg2+ acts as a calcium antagonist and protects vascular endothelial cells from oxidative stress. Imbalances in Mg2+ status, more frequently hypomagnesemia, inhibit glucose transporter type 4 translocation, increase insulin resistance, affect lipid metabolism, induce oxidative stress, and impair the antioxidant system of endothelial cells, In these ways, hypomagnesemia contributes to the initiation and progression of DM and its macrovascular and microvascular complications. In this review, we summarize recent advances in knowledge of the mechanisms whereby Mg2+ regulates insulin secretion and sensitivity. In addition, we discuss the future prospects for research regarding the mechanisms whereby Mg2+ status impacts DM and its complications.
Keywords: Diabetes; Gene mutation; Insulin resistance; Lipid peroxidation; Mg2+; Oxidative stress.