Diabetes mellitus is a metabolic disorder with a central theme of chronic hyperglycaemia which is due to a deficiency in insulin secretion and/or action. There are various types but type 2 is the commonest type of diabetes mellitus. The main pathophysiologic mechanisms of type 2 diabetes are insulin resistance and pancreatic β cell dysfunction. The pathophysiology of type 2 is not fully known so; different hypotheses keep coming up in the literature to explain its pathophysiology. One of these newer mechanisms to explain the pathophysiology of insulin resistance is deficiency of minerals. Magnesium is an essential mineral needed for various metabolic processes in the cells. Hypomagnesemia is more frequent in patients with type 2 diabetes and it has been linked with the pathophysiology of type 2 diabetes. Hypomagnesemia is associated with intracellular magnesium deficiency. Magnesium deficiency inside β cell is associated with reduced enzymatic activities insufficient intracellular ATP concentration leading to reduced insulin secretion. Also, magnesium deficiency in the cells is associated with impaired activities of the enzymes in the protein kinase B pathway of insulin action thereby contributing to insulin resistance. Hypomagnesemia is associated with increased production of pro-inflammatory cytokines which are the factors responsible for the low grade chronic inflammation associated with obesity and diabetes. Antioxidant activities are diminished in hypomagnesemia. These mechanisms are the possible explanations linking hypomagnesemia to the pathophysiology of type 2 diabetes mellitus.