HYPERTENSION, DIABETES-MELLITUS, AND INSULIN-RESISTANCE - THE ROLE OFINTRACELLULAR MAGNESIUM

Magnesium is one of the most abundant ions present in living cells and its plasma concentration is remarkably constant in healthy subjects. Plasma and intracellular magnesium concentrations are tightly regulate d by several factors. Among them, insulin seems to be one of the most important. In fact in vitro and in vivo studies have demonstrated that insulin may modulate the shift of magnesium from extracellular to int racellular space. Intracellular magnesium concentration has also been shown to be effective on modulating insulin action (mainly oxidative g lucose metabolism), offset calcium-related excitation-contraction coup ling, and decrease smooth cell responsiveness to depolarizing stimuli, by stimulating Ca2+-dependent K+ channels. A poor intracellular magne sium concentration, as found in noninsulin-dependent diabetes mellitus (NIDDM) and in hypertensive (HP) patients, may result in a defective tyrosine-kinase activity at the insulin receptor level and exaggerated intracellular calcium concentration. Both events are responsible for the impairment in insulin action and a worsening of insulin resistance in non-insulin-dependent diabetic and hypertensive patients. By contr ast, in NIDDM patients daily magnesium administration, restoring a mor e appropriate intracellular magnesium concentration, contributes to im prove insulin-mediated glucose uptake. Similarly, in HP patients magne sium administration may be useful in decreasing arterial blood pressur e and improving insulin-mediated glucose uptake. The benefits deriving from daily magnesium supplementation in NIDDM and HP patients are fur ther supported by epidemiological studies showing that high daily magn esium intake to be predictive of a lower incidence of NIDDM and HP. In conclusion, a growing body of studies suggest that intracellular magn esium may play a key role on modulating insulin-mediated glucose uptak e and vascular tone. We further suggest that a reduced intracellular m agnesium concentration might be the missing link helping to explain th e epidemiological association between NIDDM and hypertension. (C) 1997 American Journal of Hypertension, Ltd.