Effect of glucose/insulin infusion and magnesium supplementation on serum and muscle sodium and potassium and muscle [3H]ouabain binding capacity in Type 1 diabetes mellitus.
Glucose has recently been found to decrease muscle potassium content. The aim of this study was to evaluate the effect of the infusion of glucose and insulin and the effect of magnesium supplementation on serum and muscle sodium and potassium and muscle [3H]ouabain binding capacity in patients with Type 1 diabetes mellitus and in controls. Muscle potassium and sodium content, muscle [3H]ouabain binding capacity and serum potassium and sodium concentrations were determined in 10 patients with Type 1 diabetes mellitus and in 5 controls before and after an euglycaemic, hyperinsulinaemic clamp, and after an intravenous magnesium load test. Nine of the patients with Type 1 diabetes mellitus were restudied after 24 weeks of oral magnesium oxide supplementation. Basic serum and muscle sodium and potassium and muscle [3H]ouabain binding capacity did not differ between groups. The infusion of glucose and insulin reduced muscle potassium content, whereas muscle sodium content was unchanged. There were no differences between groups. Oral magnesium oxide supplementation increased muscle potassium content by 6%. Muscle [3H]ouabain binding capacity was unchanged. In patients with Type 1 diabetes mellitus, the intravenous infusion of magnesium increased serum potassium concentration before but not after oral magnesium oxide supplementation. In controls, the infusion of magnesium did not affect serum potassium concentration. It was found that intravenous infusion of glucose and insulin decreases muscle potassium content, probably by shifting potassium from the muscle cells to the splanchnic organs. Oral magnesium oxide supplementation increases muscle potassium content in patients with Type 1 diabetes mellitus. The increase in serum potassium concentration owing to the intravenous infusion of magnesium could be used in the evaluation of magnesium status in patients with Type 1 diabetes mellitus. This, however, requires further investigation.
Department of Clinical Biochemistry, Clinical Genetics and Clinical Pharmacology, Odense University Hospital, Odense, Denmark. msd@dadlnet.dk
M S
MS
Djurhuus
N A H
NA
Klitgaard
K K
KK
Pedersen
D000328:Adult; D003922:Diabetes Mellitus, Type 1 / Q000097:blood*; D005260:Female; D015309:Glucose Clamp Technique; D006801:Humans; D007262:Infusions, Intravenous; D008274:Magnesium / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000201:enzymology*; D010042:Ouabain / Q000378:metabolism; D011188:Potassium / Q000097:blood*; D012964:Sodium / Q000097:blood*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D014316:Tritium
D014316:Tritium; D010042:Ouabain; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D008274:Magnesium; D011188:Potassium