Fasting-induced G0/G1 switch gene 2 and FGF21 expression in the liver are under regulation of adipose tissue derived fatty acids

摘要

class="kwd-title">Abbreviations: AT, Adipose tissue; FA(s), fatty acid(s); TG, triacylglycerol; CGI-58, comparative gene identification-58; ATGL, Adipose triglyceride lipase; CGI-58-ATko, AT-selective ablation of CGI-58; ATGL-ATko, AT-specific deficiency of ATGL; LD, lipid droplet; NAFLD, nonalcoholic fatty liver disease; NLSD, Neutral lipid storage disease; PPARα, peroxisome proliferator-activated receptor alpha; CREBH, cAMP-responsive element binding protein, hepatocyte specific; G0S2, G0/G1 Switch Gene 2; FGF21, fibroblast growth factor 21; PGC-1α, PPARgamma co-activator-1alpha; HNF4α, hepatocyte nuclear factor 4alpha; PEPCK, Phosphoenolpyruvate carboxykinase; G6Pase, Glucose-6-phosphatase; ER, endoplasmic reticulum class="kwd-title">Keywords: Hepatic steatosis, G0/G1 switch gene 2, Fibroblast growth factor 21, CGI-58, ATGL, Lipolysis, PPARα, CREBH, Obesity class="head no_bottom_margin" id="idm140511737977824title">AbstractBackground & AimsAdipose tissue (AT)-derived fatty acids (FAs) are utilized for hepatic triacylglycerol (TG) generation upon fasting. However, their potential impact as signaling molecules is not established. Herein we examined the role of exogenous AT-derived FAs in the regulation of hepatic gene expression by investigating mice with a defect in AT-derived FA supply to the liver.