The possible role of Mg in the pathogenesis of
vascular disease has recently received increasing attention. Accumulating evidence indicates that Mg strongly influences vascular tone and responsiveness to pressor agents and that Mg deficiency may be associated with an increased risk of
hypertension. Moreover, experimental Mg deficiency produces vascular lesions with calcifications while increasing the dietary intake of Mg has been shown to prevent
atheroma and thrombotic complications. The modifications of lipid metabolism during experimental Mg deficiency have been recently characterized. Severe Mg deficiency in weanling rats produces a marked
hypertriglyceridemia and a decrease in the percentage of
cholesterol transported by
high-density lipoprotein. The decreased clearance of circulating
triglycerides appears to be the major mechanism contributing to
hyperlipemia. The same animals were found to have a reduced
insulin response after intravenous
glucose challenge and a slight reduction in
heparin release
lipoprotein lipase. A marked reduction in plasma activity of LCAT and a significant decrease in esterified/total plasma
cholesterol ratio have also been reported. Severe Mg deficiency in weanling rats produces marked changes in the
fatty acid pattern of total plasma
lipids, as shown by decreased levels of
stearic acid, increased of
oleic acid and
linoleic acid, and decreased levels of
arachidonic acid. Platelets from Mg-deficient rats become more sensitive to
thrombin. Such an increased sensitivity of platelets may in turn play an important role in initiating the vascular lesion as well as in thrombotic complications. In view of these experimental data in animal models, more work seems necessary in man to assess the effect of Mg on lipid metabolism and
vascular disease.