摘要
Nonalcoholic fatty liver disease （NAFLD） covers a spectrum of liver disorders ranging from simple steatosis to advanced pathologies, including nonalcoholic steatohepatitis and cirrhosis. NAFLD significantly contributes to morbidity and mortality in developed societies. Insulin resistance associated with central obesity is the major cause of hepatic steatosis, which is characterized by excessive accumulation of triglyceride-rich lipid droplets in the fiver. Accumulating evidence supports that dysregulation of adipose lipolysis and liver de novo lipogenesis （DNL） plays a key role in driving hepatic steatosis. In this work, we reviewed the molecular mechanisms responsible for enhanced adipose lipolysis and increased hepatic DNL that lead to hepatic lipid accumulation in the context of obesity. Delineation of these mechanisms holds promise for developing novel avenues against NAFLD.
Nonalcoholic fatty liver disease （NAFLD） covers a spectrum of liver disorders ranging from simple steatosis to advanced pathologies, including nonalcoholic steatohepatitis and cirrhosis. NAFLD significantly contributes to morbidity and mortality in developed societies. Insulin resistance associated with central obesity is the major cause of hepatic steatosis, which is characterized by excessive accumulation of triglyceride-rich lipid droplets in the fiver. Accumulating evidence supports that dysregulation of adipose lipolysis and liver de novo lipogenesis （DNL） plays a key role in driving hepatic steatosis. In this work, we reviewed the molecular mechanisms responsible for enhanced adipose lipolysis and increased hepatic DNL that lead to hepatic lipid accumulation in the context of obesity. Delineation of these mechanisms holds promise for developing novel avenues against NAFLD.
基金
Acknowledgements This work was supported by funds from the National Natural Science Foundation of China [award numbers 81270482 （to L.G.） and 81372270 （to B.X.）] and the National Institutes of Health [award number R01DK085176 （to L.Y.）].
