ArticleAmerican journal of physiology. Endocrinology and metabolism2016
Bile acids induce uncoupling protein 1-dependent thermogenesis and stimulate energy expenditure at thermoneutrality in mice.
Article in American journal of physiology. Endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 89 citations in OpenAlex.
- Changes in circulating bile acid levels during cold exposure are associated with brown adipose tissue in humans: a secondary analysis from the ACTIBATE study.Journal of physiology and biochemistry · 2026Trial
- Alternative Receptor Signaling for the Selective and Multifaceted Regulation of Human Brown Adipocytes.International journal of molecular sciences · 2026Review
- Cold exposure remodels bile acid metabolism in a mouse strain- and tissue-specific manner.The Biochemical journal · 2026Article
- Bile acid metabolism in type 2 diabetes mellitus.Nature reviews. Endocrinology · 2025Review
- Gut‑liver axis in liver disease: From basic science to clinical treatment (Review).Molecular medicine reports · 2025Review
- Gestational hypercholanemia suppresses pregnancy-associated adipose mass increase and stimulates a pro-inflammatory environment in mice.Physiological reports · 2024Article
- CPEB2-activated Prdm16 translation promotes brown adipocyte function and prevents obesity.Molecular metabolism · 2024Article
- Keys to the switch of fat burning: stimuli that trigger the uncoupling protein 1 (UCP1) activation in adipose tissue.Lipids in health and disease · 2024Review
- Article
- Regulating bile acids signaling for NAFLD: molecular insights and novel therapeutic interventions.Frontiers in microbiology · 2024Review
- Brown adipose tissue: can it keep us slim? A discussion of the evidence for and against the existence of diet-induced thermogenesis in mice and men.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Promoting metabolic inefficiency for metabolic disease.iScience · 2023Review
- The role of the gut microbiota in health and cardiovascular diseases.Molecular biomedicine · 2022Review
- Browning of the white adipose tissue regulation: new insights into nutritional and metabolic relevance in health and diseases.Nutrition & metabolism · 2022Review
- Review
- Metabolic Messengers: bile acids.Nature metabolism · 2022Review
- Microbiota and body weight control: Weight watchers within?Molecular metabolism · 2022Review
- Uncoupling Protein 1 Does Not Produce Heat without Activation.International journal of molecular sciences · 2022Review
- PRMT3 inhibitor SGC707 reduces triglyceride levels and induces pruritus in Western-type diet-fed LDL receptor knockout mice.Scientific reports · 2022Article
- The Role of Bile Acid in Improving Glucose Tolerance of Non-Obese Diabetic Rats After Proximal Small Bowel Bypass.Frontiers in physiology · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been proposed that diet-induced obesity at thermoneutrality (TN; 29°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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