TRPV1 activation prevents nonalcoholic fatty liver through UCP2 upregulation in mice
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Nonalcoholic fatty liver is characterized by the fatty deformation and lipid deposition of hepatic parenchymal cells that are associated with cardiometabolic diseases. In this study, we report the effect of capsaicin on its receptor, transient receptor potential vanilloid 1 (TRPV1) cation channel, in preventing fatty liver formation. Functional TRPV1 has been detected in hepatocytes and liver tissues. TRPV1 activation by capsaicin reduced lipid accumulation and triglyceride level in the liver from wild-type (WT) mice. However, these effects were absent in the liver from TRPV1−/− mice. Chronic dietary capsaicin increased the hepatic uncoupling protein 2 (UCP2) expression in WT but not in TRPV1−/− mice (P < 0.01). We conclude that TRPV1 long-time activation might prevent high-fat diet-induced fatty liver in mice through upregulation of hepatic UCP2. Dietary capsaicin may represent a promising intervention in populations at high risk for fatty liver.
KeywordsFatty liver Capsaicin TRPV1 UCP2
We thank Lijuan Wang (Chongqing Institute of Hypertension, China) for technical assistance.
Sources of funding
This research was supported by grants from the National Natural Science Foundation of China (30890042) and the National Basic Research Program of China (2012CB517805 and 2011CB503902).
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