糖原贮积病（gsd/gsd）大鼠再喂养后的肝脏碳通量。
Hepatic carbon flux after re-feeding in the glycogen-storage-disease (gsd/gsd) rat.
作者信息
Holness M J, Palmer T N, Worrall E B, Sugden M C
机构信息
Department of Chemical Pathology, London Hospital Medical College, U.K.
出版信息
Biochem J. 1987 Dec 15;248(3):969-72. doi: 10.1042/bj2480969.
Abstract
In this study we utilized the phosphorylase b kinase-deficient (gsd/gsd) rat as a model of hepatic substrate utilization where there is a constraint on glycogenesis imposed by the maintenance of high glycogen concentrations. Glucose re-feeding of 48 h-starved gsd/gsd rats led to suppression of hepatic glucose output. In contrast with the situation in normal rats, activation of the pyruvate dehydrogenase complex and lipogenesis was observed. It is suggested that impeding glycogenic flux may divert substrate into lipogenesis, possibly via activation of the pyruvate dehydrogenase complex.
摘要
在本研究中，我们利用磷酸化酶b激酶缺陷（gsd/gsd）大鼠作为肝脏底物利用的模型，在该模型中，由于维持高糖原浓度对糖原生成产生了限制。对饥饿48小时的gsd/gsd大鼠重新喂食葡萄糖导致肝脏葡萄糖输出受到抑制。与正常大鼠的情况相反，观察到丙酮酸脱氢酶复合体的激活和脂肪生成。提示阻碍糖原生成通量可能会使底物转向脂肪生成，可能是通过激活丙酮酸脱氢酶复合体来实现的。
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