Overexpression of Protein Targeting to Glycogen (PTG) in Rat Hepatocytes Causes Profound Activation of Glycogen Synthesis Independent of Normal Hormone- and Substrate-mediated Regulatory Mechanisms

摘要: Abstract Protein targeting to glycogen (PTG), also known as PPP1R5, is a widely expressed member of growing family proteins that target protein phosphatase-1 (PP-1) particles. Because PTG binds synthase and phosphorylase kinase, it has been suggested serves “scaffold” for efficient activation synthesis. However, very little about the metabolic effects PTG. In this study, we have used recombinant adenovirus overexpress in primary rat hepatocytes, cell type with high glycogenic capacity. We find overexpression potently activates synthesis cultured hepatocytes. Surprisingly, effect observed even complete absence carbohydrates or insulin culture medium. Furthermore, glycogenolytic agents such forskolin glucagon are largely ineffective at activating degradation overexpressing though large increases cAMP levels demonstrated. These accompanied by 3.6-fold increase state 40% decrease activity. Our results consistent model which “locks” hepatocyte mode, presumably via its ability promote interaction enzymes metabolism PP-1.