Magnesium, sodium, and potassium content and [3H]ouabain binding capacity of skeletal muscle in relatives of patients with type 2 diabetes: effect of dexamethasone.

Theoretically, disturbancies in sodium (Na) and potassium (K) homeostasis and a magnesium (Mg) deficit could be possible factors in the development of obesity, type 2 diabetes, and hypertension. Therefore, we measured electrolyte content and [3H]ouabain binding capacity of skeletal muscle in 20 relatives of type 2 diabetic patients and in 20 controls before and after glucose infusion and before and after treatment with dexamethasone, which decreases insulin sensitivity. Muscle electrolyte content and [3H]ouabain binding capacity did not differ between groups. Infusion of glucose increased muscle Na content 25%, decreased muscle potassium content 9%, and muscle Mg content 5%. Muscle potassium/Mg ratio decreased only in relatives. Treatment with dexamethasone increased muscle Na content 15% and decreased muscle Mg content 7%, whereas muscle potassium/Na ratio decreased 17%. Dexamethasone increased muscle [3H]ouabain binding capacity by 42% in both groups. Basal and 1-hour intramuscular glucose content correlated inversely with basal muscle potassium/Na ratio in relatives only. In conclusion, persons who were predisposed to the development of type 2 diabetes exhibited an increased interdependency between glucose, Na, and potassium handling in skeletal muscle. Muscle Na content and [3H]ouabain binding capacity increased during treatment with dexamethasone, and muscle potassium/Na ratio decreased. Intravenous (IV) glucose injection decreases muscle Mg content, as does a decrease in insulin sensitivity, without any differences between relatives and controls. Copyright 2002, Elsevier Science (USA). All rights reserved.