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Ochratoxin A Induces Steatosis via PPARγ-CD36 Axis
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Ochratoxin A Induces Steatosis via PPARγ-CD36 Axis
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Journal Article
Ochratoxin A Induces Steatosis via PPARγ-CD36 Axis
2021
Overview
Ochratoxin A(OTA) is considered to be one of the most important contaminants of food and feed worldwide. The liver is one of key target organs for OTA to exert its toxic effects. Due to current lifestyle and diet, nonalcoholic fatty liver disease (NAFLD) has been the most common liver disease. To examine the potential effect of OTA on hepatic lipid metabolism and NAFLD, C57BL/6 male mice received 1 mg/kg OTA by gavage daily. Compared with controls, OTA increased lipid deposition and TG accumulation in mouse livers. In vitro OTA treatment also promoted lipid droplets accumulation in primary hepatocytes and HepG2 cells. Mechanistically, OTA prevented PPARγ degradation by reducing the interaction between PPARγ and its E3 ligase SIAH2, which led to activation of PPARγ signaling pathway. Furthermore, downregulation or inhibition of CD36, a known of PPARγ, alleviated OTA-induced lipid droplets deposition and TG accumulation. Therefore, OTA induces hepatic steatosis via PPARγ-CD36 axis, suggesting that OTA has an impact on liver lipid metabolism and may contribute to the development of metabolic diseases.
Publisher
MDPI AG,MDPI
Subject
/ Animals
/ Chemical and Drug Induced Liver Injury - etiology
/ Chemical and Drug Induced Liver Injury - physiopathology
/ Droplets
/ Humans
/ Lipid Metabolism - drug effects
/ Lipids
/ Liver
/ Male
/ Mice
/ Non-alcoholic Fatty Liver Disease - chemically induced
/ Non-alcoholic Fatty Liver Disease - physiopathology
/ Organs
/ OTA
/ Peroxisome proliferator-activated receptors
/ PPAR
/ Proteins
