Chen C, Williams P F, Caterson I D
Department of Endocrinology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia.
Am J Physiol. 1993 Nov;265(5 Pt 1):E743-51. doi: 10.1152/ajpendo.1993.265.5.E743.
Glycogen metabolism in the liver, skeletal muscle, cardiac muscle, and white adipose tissue was studied in gold thioglucose (GTG) obese mice after fasting and during refeeding. Prolonged (48 h) fasted control and GTG mice were refed with standard laboratory diet for 24 h. During fasting and refeeding, the changes in glycogen content and the activity of glycogen synthase I and R and phosphorylase alpha in the liver were similar in lean and GTG mice. However, the glycogen storage in the livers from GTG mice was always greater than that in lean animals. In GTG mice the activity of liver glycogen synthase I and R was significantly higher than that in lean animals 3 and 6 h after refeeding. The activity of liver phosphorylase alpha in GTG mice was higher than that in lean mice after refeeding. There were no significant differences in the glycogen content of white adipose tissue, cardiac muscle, and skeletal muscle from lean and GTG mice during the entire study. The results of this study suggest that increased glycogen storage in the liver is a major alteration in nonoxidative glucose metabolism and contributes to the development of insulin resistance and glucose intolerance in GTG obese mice.
在禁食和重新喂食后，对硫代葡萄糖金（GTG）肥胖小鼠的肝脏、骨骼肌、心肌和白色脂肪组织中的糖原代谢进行了研究。将长期（48小时）禁食的对照小鼠和GTG小鼠重新喂食标准实验室饮食24小时。在禁食和重新喂食期间，瘦小鼠和GTG小鼠肝脏中糖原含量以及糖原合酶I和R以及磷酸化酶α的活性变化相似。然而，GTG小鼠肝脏中的糖原储存量始终高于瘦动物。在重新喂食后3小时和6小时，GTG小鼠肝脏糖原合酶I和R的活性显著高于瘦动物。重新喂食后，GTG小鼠肝脏磷酸化酶α的活性高于瘦小鼠。在整个研究过程中，瘦小鼠和GTG小鼠白色脂肪组织、心肌和骨骼肌的糖原含量没有显著差异。本研究结果表明，肝脏中糖原储存增加是非氧化葡萄糖代谢的主要改变，并促成了GTG肥胖小鼠胰岛素抵抗和葡萄糖不耐受的发展。
