A small intestinal bile acid modulates the gut microbiome to improve host metabolic phenotypes following bariatric surgery

被引:5
作者
Chen, Yingjia [1 ]
Chaudhari, Snehal N. [2 ,3 ]
Harris, David A. [1 ,4 ]
Roberts, Cullen F. [1 ]
Moscalu, Andrei [1 ]
Mathur, Vasundhara [1 ]
Zhao, Lei [5 ]
Tavakkoli, Ali [1 ]
Devlin, A. Sloan [2 ]
Sheu, Eric G. [1 ]
机构
[1] Brigham & Womens Hosp, Dept Surg, Lab Surg & Metab Res, Boston, MA 02115 USA
[2] Harvard Med Sch, Dept Biol Chem & Mol Pharmacol, Blavatnik Inst, Boston, MA 02115 USA
[3] Univ Wisconsin, Dept Biochem, Madison, WI 53706 USA
[4] Univ Wisconsin, Sch Med & Publ Hlth, Dept Surg, Madison, WI 53792 USA
[5] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA
基金
美国国家卫生研究院;
关键词
LITHOCHOLIC ACID; INSULIN-RESISTANCE; OXIDATIVE STRESS; GLUCOSE; GENE; MECHANISMS; IDENTIFICATION; REMISSION; COENZYME; RECEPTOR;
D O I
10.1016/j.chom.2024.06.014
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Bariatric surgical procedures such as sleeve gastrectomy (SG) provide effective type 2 diabetes (T2D) remission in human patients. Previous work demonstrated that gastrointestinal levels of the bacterial metabolite lithocholic acid (LCA) are decreased after SG in mice and humans. Here, we show that LCA worsens glucose tolerance and impairs whole-body metabolism. We also show that taurodeoxycholic acid (TDCA), which is the only bile acid whose concentration increases in the murine small intestine post-SG, suppresses the bacterial bile acid-inducible ( bai ) operon and production of LCA both in vitro and in vivo. . Treatment of diet- induced obese mice with TDCA reduces LCA levels and leads to microbiome-dependent improvements in glucose handling. Moreover, TDCA abundance is decreased in small intestinal tissue from T2D patients. This work reveals that TDCA is an endogenous inhibitor of LCA production and suggests that TDCA may contribute to the glucoregulatory effects of bariatric surgery.
引用
收藏
页码:1315 / 1330.e5
页数:22
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