Abstract
Liver steatosis is the most common feature of metabolic syndrome, and may progress to severe disease states. LXRα promotes SREBP‐1c‐dependent lipogenesis and fat accumulation in hepatocytes. However, the effect of LXRα on autophagy in hepatocytes and the consequent changes in energy homeostasis are elusive. This study investigated the role of LXRα modulations in autophagy in association with its impact on the progression of liver steatosis. Treatment of HepG2 cells or primary hepatocytes with T0901317 (an LXRα agonist) decreased the processing of LC3‐I to LC3‐II in a time‐ or concentration‐dependent manner. The effect of LXRα on lysosomal activity from its effect on autophagosome formation was verified using immunofluorescence confocal assays. In primary hepatocytes, LXRα agonist treatment visualized decrease of autophagic flux. Consistently, either ligand activation LXRα or LXRα overexpression decreased Atg4B levels both in vitro and in vivo. Our results provide evidence that LXRα activation inhibits autophagy in hepatocytes as mediated by the inhibition of Atg4B, implying that modulation of LXRα may affect the capacity of autophagy in hepatocytes and thereby contribute to the prevention and treatment of liver steatosis.Support or Funding InformationSupported by the Korean government (NRF‐2015R1A2A1A10052663)
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