Palmer T N, Caldecourt M A, Gossain S, Mangat S, Sugden M C
Biosci Rep. 1985 May;5(5):433-8. doi: 10.1007/BF01116561.
Renal failure is associated with peripheral insulin resistance and consequent carbohydrate intolerance. This report investigates carbohydrate metabolism in vitro in epitrochlearis and hemidiaphragm muscles taken from acutely uraemic and sham-operated rats. Muscles from acutely uraemic rats (compared to those from sham-operated rats) incubated with 5 mM glucose showed increased rates of basal and insulin-stimulated glycolysis and glycogen turnover, but pyruvate dehydrogenase and tricarboxylic acid-cycle flux was not increased in uraemia. Glycolysis (but not glycogen turnover) in muscles from acutely uraemic rats tended to show decreased responsiveness to stimulation by insulin. It is concluded that acute uraemia is associated with a defect(s) in muscle that produces intrinsic insulin resistance and results in diversion of glucose (both in basal and insulin-stimulated states) from glycogen synthesis into glycolysis.
肾衰竭与外周胰岛素抵抗及随之而来的碳水化合物不耐受有关。本报告研究了取自急性尿毒症大鼠和假手术大鼠的肱桡肌和半膈肌的体外碳水化合物代谢情况。与假手术大鼠的肌肉相比，急性尿毒症大鼠的肌肉在与5 mM葡萄糖一起孵育时，基础糖酵解和胰岛素刺激的糖酵解速率以及糖原周转率均增加，但尿毒症时丙酮酸脱氢酶和三羧酸循环通量并未增加。急性尿毒症大鼠肌肉中的糖酵解（而非糖原周转）对胰岛素刺激的反应性倾向于降低。结论是，急性尿毒症与肌肉中的一种缺陷有关，这种缺陷会产生内在的胰岛素抵抗，并导致葡萄糖（在基础状态和胰岛素刺激状态下）从糖原合成转向糖酵解。
