Djurhuus M S, Klitgaard N A H, Pedersen K K
Department of Clinical Biochemistry, Clinical Genetics and Clinical Pharmacology, Odense University Hospital, Odense, Denmark.
Scand J Clin Lab Invest. 2003;63(2):93-102. doi: 10.1080/00365510310000970.
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.
最近发现葡萄糖会降低肌肉钾含量。本研究的目的是评估输注葡萄糖和胰岛素的效果以及补充镁对1型糖尿病患者和对照组血清及肌肉钠、钾含量以及肌肉[3H]哇巴因结合能力的影响。在进行正常血糖、高胰岛素钳夹试验之前和之后以及静脉注射镁负荷试验之后,测定了10例1型糖尿病患者和5例对照组的肌肉钾和钠含量、肌肉[3H]哇巴因结合能力以及血清钾和钠浓度。9例1型糖尿病患者在口服氧化镁补充剂24周后再次进行研究。两组之间的基础血清和肌肉钠、钾以及肌肉[3H]哇巴因结合能力没有差异。输注葡萄糖和胰岛素会降低肌肉钾含量,而肌肉钠含量不变。两组之间没有差异。口服氧化镁补充剂使肌肉钾含量增加了6%。肌肉[3H]哇巴因结合能力未改变。在1型糖尿病患者中,静脉注射镁在口服氧化镁补充剂之前会增加血清钾浓度,但之后不会。在对照组中,输注镁不会影响血清钾浓度。研究发现,静脉输注葡萄糖和胰岛素可能通过将钾从肌肉细胞转移至内脏器官而降低肌肉钾含量。口服氧化镁补充剂可增加1型糖尿病患者的肌肉钾含量。静脉注射镁导致的血清钾浓度升高可用于评估1型糖尿病患者的镁状态。然而,这需要进一步研究。