Hörl W H, Kreusser W, Rambausek M, Heidland A, Ritz E
Miner Electrolyte Metab. 1983;9(3):113-8.
Glycogen content as well as the enzymes of glycogenolysis and glycogen synthesis were examined in myocardium, skeletal muscle, liver and kidneys of rats with dietary phosphorus deprivation. Myocardial glycogen content was decreased and this was accompanied by activation of the enzymes of glycogenolysis and inhibition of the enzymes of glycogen synthesis. Beta blockade (nadolol) abolished the effect of phosphorus depletion (PD) on myocardial glycogen metabolism, documenting that the effect of PD is mediated, at least in part, by increased sympathetic activity. Furthermore, administration of insulin caused a marked increase of glycogen content in the heart of both control and phosphorus-depleted (PD) animals. There was no change of glycogen content or the activities of enzymes of glycogen metabolism in skeletal muscle or kidney, but a decrease of glycogen content of the liver was observed in PD animals.
对饮食中磷缺乏的大鼠的心肌、骨骼肌、肝脏和肾脏中的糖原含量以及糖原分解和糖原合成的酶进行了检测。心肌糖原含量降低,同时伴有糖原分解酶的激活和糖原合成酶的抑制。β受体阻滞剂(纳多洛尔)消除了磷缺乏(PD)对心肌糖原代谢的影响,证明PD的作用至少部分是由交感神经活动增加介导的。此外,给予胰岛素导致对照动物和磷缺乏(PD)动物心脏中的糖原含量显著增加。骨骼肌或肾脏中的糖原含量或糖原代谢酶的活性没有变化,但在PD动物中观察到肝脏糖原含量降低。