Abstract
Magnesium (Mg(2+)) is an enzyme co-factor that plays a key role in many biochemical reactions, as well as in glucose metabolism. Clinical evidences have demonstrated that depletion of serum Mg(2+) increases exponentially with the duration of type 2 diabetes mellitus (T2DM). Diabetes is associated with low Mg(2+), and hypomagnesemia is associated with insulin resistance, inflammation, and increased risk for cardiovascular disease. In subjects at high risk of inflammation and insulin resistance, supplementation of Mg(2+) alone ameliorates both phenotypes, slowing the development and progression of hepatic steatosis. We analyze the relationship between serum Mg(2+) levels and the onset of T2DM in a large cohort of well-characterized adult white individuals participating in the CATAMERI study, who were reexamined after a mean follow-up of 5.6 ± 0.9 years. In our analysis we acquired a significant negative correlation between Mg(2+) levels, fasting glucose, and 2h-post load glucose in subjects who underwent an OGTT. Moreover, Mg(2+) levels correlated negatively with fasting insulin levels, and positively with the lipid profile. As for the detrimental effect of lower circulating Mg(2+) levels, our data revealed a significant reduction of T2DM risk of about 20% for each 1 mg/dL increase of circulating Mg(2+). The present results are consistent with the theory that Mg(2+) supplementation could ameliorate insulin sensitivity reducing the risk to develop T2DM.