肥胖高血糖小鼠肝脏糖原合成中葡萄糖激活功能的缺陷
Defective activation by glucose of hepatic glycogen synthesis in the obese hyperglycaemic mouse.
作者信息
Smith S A, Cawthorne M A, Levy A L, Simson D L
出版信息
Biochem J. 1983 Nov 15;216(2):491-4. doi: 10.1042/bj2160491.
Abstract
The administration of an oral glucose load to 24 h-starved lean (+/?) male C57BL/6 mice produced a rapid, 7-fold increase in the rate of hepatic glycogen synthesis and a sustained activation of glycogen synthase. In contrast, glucose produced only a small (4.5-fold), short-lived increase in hepatic glycogen synthesis in genetically obese (ob/ob) mice and no activation of glycogen synthase.
摘要
给禁食24小时的瘦型（+/？）雄性C57BL/6小鼠口服葡萄糖后，肝糖原合成速率迅速增加了7倍，糖原合酶持续激活。相比之下，葡萄糖仅使遗传性肥胖（ob/ob）小鼠的肝糖原合成有小幅（4.5倍）、短暂的增加，且未激活糖原合酶。
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