A mechanism of regulation of hepatic Fru 2,6-P2 concentration upon refeeding: involvement of xylulose 5-P and cyclic-AMP.
A mechanism of regulation of hepatic Fru 2,6-P2 concentration upon refeeding: involvement of xylulose 5-P and cyclic-AMP.
复制标题
再喂食时肝脏 Fru 2,6-P2 浓度的调节机制：木酮糖 5-P 和环 AMP 的参与。
DOI：
10.1006/bbrc.1996.0634
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发表时间：
1996
影响因子：
3.1
通讯作者：
K. Uyeda
中科院分区：
文献类型：
--
作者：
Y. Liu;K. Uyeda
为了确定再喂养大鼠肝脏中果糖2，6-P2延迟增加的机制，研究了再喂养NIH或高糖饮食后各种代谢产物变化的时间过程。在饥饿48 h的大鼠肝脏中，果糖2，6-P2和木酮糖5-P的增加动力学相似，但不同于己糖6-P或糖原。果糖2，6-P2水平的增加是果糖6-P、2-激酶和果糖2，6-二磷酸酶活性比率变化的组合的结果，表明双功能酶的去磷酸化和cAMP降低。果糖2，6-P2和木酮糖5-P与去磷酸化之间的类似相关性在再喂食高糖饮食和饥饿16 h的大鼠中观察到。这些动力学结果与以下想法一致：由木酮糖5-P激活的特异性蛋白磷酸酶2A使果糖6-P，2-激酶：果糖2，6-二磷酸酶去磷酸化，并且还降低蛋白激酶A活性，导致肝果糖2，6-P2增加。
In order to determine the mechanism for delayed increase in Fructose 2,6-P2 in livers of refed rats, the time course of changes in various metabolites upon refeeding NIH or high sucrose diet was investigated. Kinetics of increase in Fructose 2,6-P2 and Xylulose 5-P were similar but different from hexose 6-P or glycogen in the livers of 48 h starved rats refed with NIH diet. The increase in the Fructose 2,6-P2 level was a result of a combination of changes in Fructose 6-P,2-kinase and Fructose 2,6-bisphosphatase activity ratios, indicating dephosphorylation of the bifunctional enzyme and decreased cAMP. A similar correlation between Fructose 2,6-P2 and Xylulose 5-P and dephosphorylation was observed with refeeding high sucrose diet and also with 16 h starved rats. These kinetic results are consistent with the idea that a specific protein phosphatase 2A, activated by Xylulose 5-P, dephosphorylates Fructose 6-P,2-kinase:Fructose 2,6-bisphosphatase and also decreased protein kinase A activity, resulting in increased hepatic Fructose 2,6-P2.