The SCAP/SREBP Pathway: A Mediator of Hepatic Steatosis.
- Author:
Young Ah MOON
1
Author Information
- Publication Type:Review
- Keywords: Non-alcoholic fatty liver disease; Insulin resistance; Hypertriglyceridemia; Lipogenesis
- MeSH: Animals; Dyslipidemias; Fibrosis; Hepatocytes; Hypertriglyceridemia; Inflammation; Insulin Resistance; Lipogenesis; Liver; Non-alcoholic Fatty Liver Disease; Obesity; Transcription Factors; Triglycerides
- From:Endocrinology and Metabolism 2017;32(1):6-10
- CountryRepublic of Korea
- Language:English
- Abstract: Nonalcoholic fatty liver disease (NAFLD) is strongly associated with insulin resistance, obesity, and dyslipidemia. NAFLD encompasses a wide range of states from the simple accumulation of triglycerides in the hepatocytes to serious states accompanied by inflammation and fibrosis in the liver. De novo lipogenesis has been shown to be a significant factor in the development of hepatic steatosis in insulin-resistant states. Sterol regulatory element binding protein-1c (SREBP-1c) is the main transcription factor that mediates the activation of lipogenesis, and SREBP cleavage activating protein (SCAP) is required for the activation of SREBPs. Here, recent animal studies that suggest SCAP as a therapeutic target for hepatic steatosis and hypertriglyceridemia are discussed.
