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正常甲状腺和甲状腺功能亢进大鼠再喂食后肝脏中果糖-2,6-二磷酸浓度及脂肪生成的调节。糖原生成的调节作用。

Regulation of hepatic fructose 2,6-bisphosphate concentrations and lipogenesis after re-feeding in euthyroid and hyperthyroid rats. A regulatory role for glycogenesis.

作者信息

Holness M J, Cook 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. 1988 Jun 1;252(2):357-62. doi: 10.1042/bj2520357.

Abstract

The time courses of restoration of fructose 2,6-bisphosphate (Fru-2,6-P2) concentrations and rates of lipogenesis after chow re-feeding were correlated with glycogen concentrations and rates of glycogen synthesis in livers of 48 h-starved euthyroid and hyperthyroid rats. Although a regulatory function for glycogen in the regulation of Fru-2,6-P2 concentrations was excluded, an inverse relationship between rates of glycogenesis and Fru-2,6-P2 concentrations indicated a role for glycogenesis in the suppression of Fru-2,6-P2 concentrations during the early (0-4 h) period of re-feeding. There was also a negative correlation between rates of glycogenesis and lipogenesis, and a positive correlation between glycogen concentrations and the lipogenic rate. Decreased rates of glycogenesis in hyperthyroid rats were associated with increased rates of lipogenesis. The response of Fru-2,6-P2 to changes in the glycogenic rate was modified by hyperthyroidism, although a negative correlation was again observed.

摘要

在重新喂食普通饲料后,48小时饥饿的正常甲状腺和甲状腺功能亢进大鼠肝脏中果糖2,6 - 二磷酸(Fru - 2,6 - P2)浓度的恢复时间进程以及脂肪生成速率与糖原浓度和糖原合成速率相关。尽管排除了糖原在调节Fru - 2,6 - P2浓度方面的调节功能,但糖原生成速率与Fru - 2,6 - P2浓度之间的负相关表明,在重新喂食的早期(0 - 4小时),糖原生成在抑制Fru - 2,6 - P2浓度方面发挥了作用。糖原生成速率与脂肪生成速率之间也存在负相关,而糖原浓度与脂肪生成速率之间存在正相关。甲状腺功能亢进大鼠中糖原生成速率的降低与脂肪生成速率的增加有关。尽管再次观察到负相关,但甲状腺功能亢进改变了Fru - 2,6 - P2对糖原生成速率变化的反应。

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