Animal Cells and Systems, 2014, 01, 77─82

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

YooJeong Lee, Jung Hwan Yu, Won-Ho Kim, Jae-woo Kim

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 tranional 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.

• ISBN or ISSN: 1976-8354

• 본 연구는 질병관리본부 연구개발과제(과제번호 2011-NG64001-00) 연구비를 지원받아 수행되었습니다.
• This research was supported by a fund(code 2011-NG64001-00) by Research of Korea Centers for Disease Control and Prevention.