Abstract
Crossing the Rubicon: Adipose Tissue Autophagy Breaks Out NAFLD
Highlights
The spectrum of N onalcoholic fatty liver disease (NAFLD) ranges from simple steatosis to nonalcoholic steatohepatitis that manifests as fatty liver with hepatic injury, inflammation, and fibrosis, which may further progress to cirrhosis and even hepatocellular carcinoma
An increase in free fatty acid (FFA) uptake from the systemic circulation because of increased lipolysis in adipose tissue and from the diet leads to the accumulation of hepatic triglycerides, contributing to NAFLD development
Enhanced autophagy-mediated lipolysis leads to decreased lipid accumulation in adipocytes and increased FFA levels in the circulation, promoting the flux of FFA into hepatocytes, resulting in the increased fat accumulation in the liver
Summary
The spectrum of NAFLD ranges from simple steatosis to nonalcoholic steatohepatitis that manifests as fatty liver with hepatic injury, inflammation, and fibrosis, which may further progress to cirrhosis and even hepatocellular carcinoma. An increase in free fatty acid (FFA) uptake from the systemic circulation because of increased lipolysis in adipose tissue and from the diet leads to the accumulation of hepatic triglycerides, contributing to NAFLD development. Autophagy is a mechanism of clearing accumulated intracellular lipids, and its suppression in chronic liver disease is associated with lipid deposition in the development of NAFLD.
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