Pathophysiology of Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis.
Publication Title
Clinics in liver disease
Document Type
Article
Publication Date
2-1-2018
Keywords
Fibrosis; Genetic factors; Inflammation; Nonalcoholic fatty liver disease (NAFLD); Nonalcoholic steatohepatitis (NASH); Adipokines/metabolism; Adipose Tissue/physiopathology; Endoplasmic Reticulum Stress; Hepatic Stellate Cells/physiology; Humans; Iron/metabolism; Kupffer Cells/physiology; Lipid Metabolism; Macrophages/physiology; Non-alcoholic Fatty Liver Disease/etiology; Non-alcoholic Fatty Liver Disease/genetics; Non-alcoholic Fatty Liver Disease/physiopathology; Oxidative Stress
Abstract
Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of liver disorders ranging from hepatic steatosis to nonalcoholic steatohepatitis (NASH) and ultimately may lead to cirrhosis. Hepatic steatosis or fatty liver is defined as increased accumulation of lipids in hepatocytes and results from increased production or reduced clearance of hepatic triglycerides or fatty acids. Fatty liver can progress to NASH in a significant proportion of subjects. NASH is a necroinflammatory liver disease governed by multiple pathways that are not completely elucidated. This review describes the main mechanisms that have been reported to contribute to the pathophysiology of NAFLD and NASH.
Clinical Institute
Digestive Health
Specialty/Research Institute
Gastroenterology
