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

Animal Cells and Systems 2014년 18권 2호 p.77 ~ 82
이유정, 유정환, 김원호, 김재우,
소속 상세정보
이유정 ( Lee Yoo-Jeong ) - National Institutes of Health Center for Biomedical Sciences Division of Metabolic Diseases
유정환 ( Yu Jung-Hwan ) - Yonsei University College of Medicine Department of Biochemistry and Molecular Biology
김원호 ( Kim Won-Ho ) - National Institutes of Health Center for Biomedical Sciences Division of Metabolic Diseases
김재우 ( Kim Jae-Woo ) - Yonsei University College of Medicine Department of Biochemistry and Molecular Biology

Abstract


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.

키워드

nonalcoholic fatty liver disease; hepatic steatosis; lipid accumulation; PPARγ, MGAT1

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