Title

Pathophysiology of Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis.

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

Department

Gastroenterology

Volume

22

Issue

1

First Page

23

Last Page

37

PubMed ID

29128059

Journal Title

Clinics in liver disease

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