title: Magnesium, sodium, and potassium content and [3H]ouabain binding capacity of skeletal muscle in relatives of patients with type 2 diabetes: effect of dexamethasone.
abstract: 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.
authors.affiliation: Department of Clinical Biochemistry, Odense University Hospital, Odense, Denmark.
authors.forename: M S
authors.initials: MS
authors.lastname: Djurhuus
authors.forename: J E
authors.initials: JE
authors.lastname: Henriksen
authors.forename: N A H
authors.initials: NA
authors.lastname: Klitgaard
mesh_terms: D000293:Adolescent; D000328:Adult; D001834:Body Water / Q000378:metabolism; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology*; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism*; D005260:Female; D005947:Glucose; D005951:Glucose Tolerance Test; D006706:Homeostasis / Q000187:drug effects; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D008274:Magnesium / Q000378:metabolism*; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism*; D010042:Ouabain / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D012727:Sex Characteristics; D012964:Sodium / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
chemical_list: D010042:Ouabain; D003907:Dexamethasone; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D008274:Magnesium; D005947:Glucose; D011188:Potassium