TRPV1 activation prevents nonalcoholic fatty liver through UCP2 upregulation in mice
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
- 6.Ma ST, Zhang LL, Yang DC, Ma LQ, Luo ZD, Liu DY, Zhu ZM (2010) Dietary capsaicin upregulates uncoupling protein 2/3 expression in visceral adipose tissue and enhances acetylcholine-induced hypotensive effect in mice. Prog Nutr 12:19–23Google Scholar
- 11.Mulvihill EE, Allister EM, Sutherland BG, Telford DE, Sawyez CG, Edwards JY, Markle JM, Hegele RA, Huff MW (2009) Naringenin prevents dyslipidemia, apolipoprotein B overproduction, and hyperinsulinemia in LDL receptor-null mice with diet-induced insulin resistance. Diabetes 58:2198–2210PubMedCrossRefGoogle Scholar