MAGNESIUM-DEFICIENCY PRODUCES INSULIN-RESISTANCE AND INCREASED THROMBOXANE SYNTHESIS

Evidence suggests that magnesium deficiency may play an important role in cardiovascular disease. In this study, we evaluated the effects of a magnesium infusion and dietary-induced isolated magnesium deficienc y on the production of thromboxane and on angiotensin II-mediated aldo sterone synthesis in normal human subjects. Because insulin resistance may be associated with altered blood pressure, we also measured insul in sensitivity using an intravenous glucose tolerance test with minima l model analysis in six subjects. The magnesium infusion reduced urina ry thromboxane concentration and angiotensin II-induced plasma aldoste rone levels. The low magnesium diet reduced both serum magnesium and i ntracellular free magnesium in red blood cells as determined by nuclea r magnetic resonance (186+/-10 [SEM] to 127+/-9 mM, p<0.01). Urinary t hromboxane concentration measured by radioimmunoassay increased after magnesium deficiency. Similarly, angiotensin II-induced plasma aldoste rone concentration increased after magnesium deficiency. Analysis show ed that all subjects studied had a decrease in insulin sensitivity aft er magnesium deficiency (3.69+/-0.6 to 2.75+/-0.5 min-1 per microunit per milliliter X 10(4), p<0.03). We conclude that dietary-induced magn esium deficiency 1) increases thromboxane urinary concentration and 2) enhances angiotensin-induced aldosterone synthesis. These effects are associated with a decrease in insulin action, suggesting that magnesi um deficiency may be a common factor associated with insulin resistanc e and vascular disease.