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New mechanisms contributing to hepatic steatosis: glucose, insulin, and lipid signaling

 Yoo Jeong Lee  ;  Jung Hwan Yub  ;  Won-Ho Kim  ;  Jae-woo Kim 
 Animal Cells and Systems, Vol.18(2) : 77-82, 2014 
Journal Title
 Animal Cells and Systems 
Issue Date
nonalcoholic fatty liver disease ; hepatic steatosis ; lipid accumulation ; PPARγ ; MGAT1
Nonalcoholic fatty liver disease (NAFLD) is the most common type of chronic liver disease and can lead to hepatic cirrhosis with liver failure. NAFLD is common in individuals who have obesity, diabetes, dyslipidemia, and/or hypertension. NAFLD comprises a wide spectrum of liver lesions ranging from mild hepatic steatosis to nonalcoholic steatohepatitis (NASH), the most aggressive form. Hepatic steatosis, also called fatty liver, is the hallmark of NAFLD and is defined as excess intrahepatic triglyceride (TG) content (≥5% of liver volume or weight). In some cases, the fat accumulation is associated with steatohepatitis, inflammation, and fibrous change of the liver. Studies on the regulation of de novo fatty acid synthesis have revealed the mechanism leading to hepatic steatosis, mostly emphasizing the roles of transcriptional regulation of enzymes involved in lipid metabolic pathway. Recently, high-fat diet-induced hepatic lipid accumulation has also been associated with hepatocyte uptake of fatty acids from lipolyzed TG in adipose tissue, as well as hepatic TG incorporation. This review discusses a conceptual framework of how hepatic TG accumulation contributes to hepatic steatosis.
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1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Jae Woo(김재우) ORCID logo https://orcid.org/0000-0001-5456-9495
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