Triscari J, Stern J S, Johnson P R, Sullivan A C
Metabolism. 1979 Feb;28(2):183-9. doi: 10.1016/0026-0495(79)90084-2.
Carbohydrate metabolism was evaluated in lean and obese Zucker rats. Plasma glucose concentration, renal and hepatic gluconeogenesis, and hepatic glycogen content and rates of synthesis were investigated in 2-mo and 8-mo-old animals. Mild hyperglycemia was observed in obese Zucker rats compared to lean rats and was more pronounced in males than in females. Rates of glucose disappearance were normal in both female and male rats, although there was a trend toward decreased clearance in the male. Total organ hepatic and kidney PEPCK activity and kidney glucose production were elevated in obese compared to lean rats. Total organ hepatic glycogen levels and rates of glycogen synthesis were increased significantly in obese compared to lean, the increase being greater in males than females. The mild hyperglycemia present in obese Zucker rats is not associated with delayed disappearance of intravenously administered glucose, but may be due to the increased production of glucose by whole kidney and liver.
对瘦型和肥胖型 Zucker 大鼠的碳水化合物代谢进行了评估。在 2 月龄和 8 月龄的动物中研究了血浆葡萄糖浓度、肾和肝糖异生、肝糖原含量及合成速率。与瘦型大鼠相比,肥胖型 Zucker 大鼠出现轻度高血糖,且在雄性中比雌性更明显。雌性和雄性大鼠的葡萄糖消失率均正常,尽管雄性有清除率降低的趋势。与瘦型大鼠相比,肥胖大鼠的全器官肝和肾磷酸烯醇式丙酮酸羧激酶(PEPCK)活性及肾葡萄糖生成增加。与瘦型大鼠相比,肥胖大鼠的全器官肝糖原水平及糖原合成速率显著增加,雄性的增加幅度大于雌性。肥胖型 Zucker 大鼠中存在的轻度高血糖与静脉注射葡萄糖的消失延迟无关,而可能是由于全肾和肝脏葡萄糖生成增加所致。