Pathophysiology of Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis

Clin Liver Dis. 2018 Feb;22(1):23-37. doi: 10.1016/j.cld.2017.08.007. Epub 2017 Oct 18.

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.

Keywords: Fibrosis; Genetic factors; Inflammation; Nonalcoholic fatty liver disease (NAFLD); Nonalcoholic steatohepatitis (NASH).

Publication types

  • Review

MeSH terms

  • 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

Substances

  • Adipokines
  • Iron