糖原
内科学
内分泌学
糖原磷酸化酶
葡萄糖稳态
糖原合酶
生物
糖原脱支酶
糖原贮积病
每2
碳水化合物代谢
昼夜节律
糖尿病
医学
生物钟
胰岛素抵抗
时钟
作者
Fabio Zani,Ludovic Breasson,Barbara Becattini,Ana Vukolic,Jean‐Pierre Montani,Urs Albrecht,Alessandro Provenzani,Juergen Ripperger,Giovanni Solinas
标识
DOI:10.1016/j.molmet.2013.06.006
摘要
The interplay between hepatic glycogen metabolism and blood glucose levels is a paradigm of the rhythmic nature of metabolic homeostasis. Here we show that mice lacking a functional PER2 protein (Per2Brdm1) display reduced fasting glycemia, altered rhythms of hepatic glycogen accumulation, and altered rhythms of food intake. Per2Brdm1 mice show reduced hepatic glycogen content and altered circadian expression during controlled fasting and refeeding. Livers from Per2Brdm1 mice display reduced glycogen synthase protein levels during refeeding, and increased glycogen phosphorylase activity during fasting. The latter is explained by PER2 action on the expression of the adapter proteins PTG and GL, which target the protein phosphatase-1 to glycogen to decrease glycogen phosphorylase activity. Finally, PER2 interacts with genomic regions of Gys2, PTG, and GL. These results indicate an important role for PER2 in the hepatic transcriptional response to feeding and acute fasting that promotes glucose storage to liver glycogen.
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