New experimental data on the relationship between diabetes mellitus and magnesium.

ABSTRACT

Diabetes mellitus is the most frequent chronic disease associated with secondary magnesium deficit. Hypomagnesaemia is a central feature of the deficit, which is often reported in experimental and clinical forms of the disease. In diabetic rats as in man, plasma magnesium concentrations may correlate inversely with the degree of hyperglycaemia. The duration of the disease also appears to be relevant. The hypomagnesaemia of diabetes might be expected to affect intracellular concentrations of the ion. However, although some animal and clinical studies have reported subnormal magnesium concentrations in blood cells, bone, and soft tissues of diabetics, the relationship between plasma magnesium concentration and intracellular level of the ion is inconsistent. Clinical studies have speculated on a potential link between the magnesium deficit of diabetes and several diabetic complications, including cardiovascular problems and retinopathy. Recent experimental studies are largely supportive of such a link; myocardial disorders associated with magnesium deficiency have been reported in diabetic mice and rabbits. It is possible that a common mechanism involving magnesium may be responsible for some of the diverse complications of diabetes. The aetiology of hypomagnesaemia in diabetes is complex. Nevertheless, plasma magnesium concentrations are ultimately determined by four processes intake, gastrointestinal absorption, redistribution within body pools, and urinary excretion. This review considers in turn the potential role of each of these processes in the development of diabetic hypomagnesaemia. Both experimental and clinical studies suggest that hypermagnesiuria may be the major factor involved. Recent animal studies have described a specific renal tubular magnesium defect in diabetes, which, together with the osmotic diuresis, is responsible for large magnesium losses. The precise cause of the defect is unknown, but it may relate to the prolonged hyperglycaemia, insulinopenia, disturbance of phosphate metabolism, or other hormonal changes which characterize the disease.