Effect of Magnesium Administration in Subjects With Family History of Diabetes or Metabolic Syndrome

Magnesium is the second most abundant ion in human cells and plays fundamental roles in several enzymatic reactions: it is involved in ATP production, in the phosphorylation of proteins, in glucose metabolism and in the contraction of cytoskeleton.

Several epidemiological studies demonstrated that low dietary magnesium intake is inversely associated with diabetes mellitus, hypertension and metabolic syndrome.

Magnesium could be related to important haemodynamic and metabolic anomalies: at vascular level it acts as an antagonist of calcium, especially in vascular smooth muscle cells, thus its deficit could enhance vascular contraction; with regard to glucose metabolism, magnesium is involved in the physiopathological mechanism of insulin resistance, through a reduction in cellular uptake of glucose. This condition and the subsequent compensatory hyperinsulinemia can ultimately lead to increased synthesis of proinflammatory cytokines and to endothelial dysfunction. Thus, magnesium depletion and subsequent alterations can increase the risk of developing vascular disease such as atherosclerosis and has been associated with cardiovascular events.

Several clinical trials have explored the possible beneficial effect of magnesium supplementation on blood pressure, plasma lipids and insulin resistance but the results are often contradictory. One of the possibilities for these unclear results could be that in some of them the interventions started too late when haemodynamic and metabolic changes are more difficult to revert.

The investigators hypothesis is that magnesium supplementation in a population at increased genetic risk of developing metabolic syndrome but without it could improve blood pressure and the other metabolic syndrome related components.

Thus, the aim of the present study is to evaluate the effect of oral supplementation of magnesium (16.2 mmol/day of magnesium pidolate) on metabolic syndrome's components in a sample of 15 subjects who are at increased risk of developing metabolic syndrome since have a positive familiar history of type II diabetes mellitus and/or metabolic syndrome(AHA/NHLBI criteria).