New mechanisms contributing to hepatic steatosis: glucose, insulin, and lipid signaling

초록

Nonalcoholic fatty liver disease (NAFLD) is the most common type of chronic liver disease and can lead to hepaticcirrhosis with liver failure. NAFLD is common in individuals who have obesity, diabetes, dyslipidemia, and/orhypertension. NAFLD comprises a wide spectrum of liver lesions ranging from mild hepatic steatosis to nonalcoholicsteatohepatitis (NASH), the most aggressive form. Hepatic steatosis, also called fatty liver, is the hallmark of NAFLD and isdefined as excess intrahepatic triglyceride (TG) content (≥5% of liver volume or weight). In some cases, the fataccumulation is associated with steatohepatitis, inflammation, and fibrous change of the liver. Studies on the regulation ofde novo fatty acid synthesis have revealed the mechanism leading to hepatic steatosis, mostly emphasizing the roles oftranscriptional regulation of enzymes involved in lipid metabolic pathway. Recently, high-fat diet-induced hepatic lipidaccumulation has also been associated with hepatocyte uptake of fatty acids from lipolyzed TG in adipose tissue, as well ashepatic TG incorporation. This review discusses a conceptual framework of how hepatic TG accumulation contributes tohepatic steatosis.

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