Gut microbiota has emerged as a modulator of host metabolism and energy balance. However, the precise microbial metabolites mediating thermogenic activation in obesity remain largely undefined. We investigated the effect of antibiotic treatment under a high-fat diet on metabolites and its contribution to lipolysis and thermogenesis. Antibiotic treatment in high-fat diet-fed rats reduced adiposity and enhanced adaptive thermogenesis. Metabolomics revealed elevated taurine levels in the cecum content and plasma of antibiotic-treated animals, correlating with increased expressions of UCP1 and TGR5 in brown adipose tissue. Taurine enhanced lipolysis and oxygen consumption in mouse adipose tissue and human adipocytes. Thereby, taurine modulated lipolysis dependent on TGR5 signaling in adipose tissue. Human data confirmed that taurine promotes browning of white adipocytes and that acute cold exposure leads to a marked drop in circulating taurine, suggesting its rapid recruitment into thermogenic tissues. Besides its synthesis in the liver and dietary uptake, taurine can be a microbiota-derived metabolite that activates adipose thermogenesis and lipolysis through TGR5 and possibly taurine transporter-dependent mechanisms. These findings uncover a gut-adipose axis with therapeutic potential for metabolic disease.
Antibiotic-Mediated Modulation of the Gut Microbiome Identifies Taurine as a Modulator of Adipocyte Function Through TGR5 Signaling.
阅读:6
作者:Jäger Elisabeth, Peeva Viktoriya, Gnad Thorsten, Haange Sven-Bastiaan, Rolle-Kampczyk Ulrike, Stäubert Claudia, Krumbholz Petra, Heiker John T, Gebhardt Claudia, Krügel Ute, Sen Paromita, Harazin Monika, Stab Viktoria, Münzker Julia, Hamdani Nazha, Pfeifer Alexander, von Bergen Martin, Till Andreas, Fenske Wiebke K
| 期刊: | International Journal of Molecular Sciences | 影响因子: | 4.900 |
| 时间: | 2026 | 起止号: | 2026 Jan 16; 27(2):917 |
| doi: | 10.3390/ijms27020917 | ||
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
