College of Pharmacy, Xinjiang Medical University, Urumqi, China.
Nanshan Hospital, The First Affiliated Hospital of Guangzhou University of Chinese Medicine (Shenzhen Nanshan Hospital of Chinese Medicine), Shenzhen, China.
Gut Microbes. 2023 Jan-Dec;15(1):2192155. doi: 10.1080/19490976.2023.2192155.
Accumulating evidence suggests that the bile acid regulates type 2 diabetes mellitus (T2DM) through gut microbiota-host interactions. However, the mechanisms underlying such interactions have been unclear. Here, we found that glycoursodeoxycholic acid (GUDCA) positively regulates gut microbiota by altering bile acid metabolism. GUDCA in mice resulted in higher taurolithocholic acid (TLCA) level and abundance. Together, these changes resulted in the activation of the adipose G-protein-coupled bile acid receptor, GPBAR1 (TGR5) and upregulated expression of uncoupling protein UCP-1, resulting in elevation of white adipose tissue thermogenesis. The anti-T2DM effects of GUDCA are linked with the regulation of the bile acid and gut microbiota composition. This study suggests that altering bile acid metabolism, modifying the gut microbiota may be of value for the treatment of T2DM.
越来越多的证据表明，胆汁酸通过肠道微生物群-宿主相互作用来调节 2 型糖尿病（T2DM）。然而，这种相互作用的机制尚不清楚。在这里，我们发现甘氨熊脱氧胆酸（GUDCA）通过改变胆汁酸代谢来正向调节肠道微生物群。GUDCA 在小鼠中导致较高的牛磺胆酸（TLCA）水平和丰度。这些变化共同导致脂肪 G 蛋白偶联胆汁酸受体，GPBAR1（TGR5）的激活和解偶联蛋白 UCP-1 的表达上调，导致白色脂肪组织产热增加。GUDCA 的抗 T2DM 作用与胆汁酸和肠道微生物群组成的调节有关。这项研究表明，改变胆汁酸代谢、修饰肠道微生物群可能对 T2DM 的治疗具有价值。
