Journal
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
Volume 310, Issue 5, Pages E346-E354Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00485.2015
Keywords
brown adipose tissue; diet-induced obesity; mitochondrial uncoupling protein 1; bile acids; thermogenesis; type 2 deidodinase
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Funding
- Foundation for Polish Science, programme WELCOME [WELCOME/2010-4/3]
- EU Structural Funds in Poland within the Innovative Economy Programme and REFRESH project [FP7-REGPOT-2010-1-264103]
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It has been proposed that diet-induced obesity at thermoneutrality (TN; 29 degrees C) is reduced by a UCP1-dependent thermogenesis; however, it has not been shown how UCP1-dependent thermogenesis can be activated in the absence of sympathetic activity. A recent study provides such a mechanism by showing that dietary bile acids (BAs) suppress obesity in mice fed a high-fat diet (HFD) by a mechanism dependent on type 2 deiodinase (DIO2); however, neither a role for UCP1 nor the influence of sympathetic activity was properly assessed. To test whether the effects of BAs on adiposity are independent of Ucp1 and cold-activated thermogenesis, obesity phenotypes were determined in C57BL6/J(+/+). (WT) and C57BL6/J. Ucp1(-/-). mice (Ucp1-KO) housed at TN and fed a HFD with or without 0.5% (wt/wt) cholic acid (CA) for 9 wk. CA in a HFD reduced adiposity and hepatic lipogenesis and improved glucose tolerance in WT but not in Ucp1-KO mice and was accompanied by increases in food intake and energy expenditure (EE). In iBAT, CA increased Ucp1 mRNA and protein levels 1.5- and twofold, respectively, and increased DIO2 and TGR5 protein levels in WT mice. Despite enhanced Dio2 expression in Ucp1-KO and Ucp1-KO-CA treated mice, this did not enhance the ability of BAs to reduce obesity. By comparing the effects of BAs on WT and Ucp1-KO mice at TN, our study showed that BAs suppress diet-induced obesity by increasing EE through a mechanism dependent on Ucp1 expression, which is likely independent of adrenergic signaling.
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