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Regulation role of CRTC3 in skeletal muscle and adipose tissue
Author(s) -
Liu Jiaqi,
Xu Ziye,
Wu Weiche,
Wang Yizhen,
Shan Tizhong
Publication year - 2018
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.25917
Subject(s) - creb , skeletal muscle , coactivator , glut4 , mitochondrial biogenesis , microbiology and biotechnology , creb1 , cyclic adenosine monophosphate , protein kinase a , adipose tissue , endocrinology , white adipose tissue , cyclic amp response element binding protein , energy homeostasis , medicine , biology , transcription factor , glucose uptake , glucose homeostasis , mitochondrion , kinase , biochemistry , insulin resistance , receptor , diabetes mellitus , insulin , gene , obesity
The cyclic adenosine monophosphate (cAMP)—protein kinase A (PKA) signaling pathway plays important role in regulating energy homeostasis. Many of the effects of the cAMP‐PKA signaling is mediated through the cAMP responsive element binding protein (CREB) and its coactivator CREB‐regulated transcription coactivators (CRTCs). CRTC3 is a member of CRTCs family proteins and plays important roles in glucose and energy metabolism. Previous studies show that global knockout of CRTC3 enhances oxygen consumption and energy expenditure and subsequently protects the knockout animal against obesity. In skeletal muscle, CRTC3 affects lipid and glycogen metabolism and mitochondrial biogenesis. In white adipocytes, CRTC3 regulates GLUT4 expression and glucose uptake. More recently, the localization and function of CRTC3 in brown fat have been reported. In this review, we mainly discuss the regulatory role of CRTC3 in skeletal muscle and adipose tissues.