Antibiotic-caused changes in intestinal flora (dysbiosis) can have various effects on the host. Secondary bile acids produced by intestinal bacteria are ligands for specific nuclear receptors, which regulate glucose, lipid, and drug metabolism in the liver. The present study aimed to clarify the effect of changes in secondary bile acids caused by antibiotic-induced dysbiosis on the host physiology, especially glucose, lipid, and drug metabolism. After oral administration of non-absorbable antibiotics for 5 days, decreased amounts of secondary bile acid-producing bacteria in faeces and a reduction in secondary bile acid [lithocholic acid (LCA) and deoxycholic acid (DCA)] levels in the liver were observed. Serum glucose and triglyceride levels were also decreased, and these decreases were reversed by LCA and DCA supplementation. Quantitative proteomics demonstrated that the expression levels of proteins involved in glycogen metabolism, cholesterol, bile acid biosynthesis, and drug metabolism (Cyp2b10, Cyp3a25, and Cyp51a1) were altered in the liver in dysbiosis, and these changes were reversed by LCA and DCA supplementation. These results suggested that secondary bile acid-producing bacteria contribute to the homeostasis of glucose and triglyceride levels and drug metabolism in the host, and have potential as therapeutic targets for treating metabolic disease.

中文翻译：

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短期抗生素引起的营养不良引起的肝次要胆汁酸的减少会降低小鼠的血清葡萄糖和甘油三酸酯水平。

抗生素引起的肠道菌群变化（营养不良）可对宿主产生多种影响。肠道细菌产生的仲胆汁酸是特定核受体的配体，这些受体调节肝脏中的葡萄糖，脂质和药物代谢。本研究旨在阐明由抗生素引起的营养不良引起的继发性胆汁酸变化对宿主生理尤其是葡萄糖，脂质和药物代谢的影响。口服非吸收性抗生素5天后，观察到粪便中产生次级胆汁酸的细菌数量减少，并且肝脏中的次级胆汁酸[lithocholic acid（LCA）和Deoxycholic acid（DCA）]水平降低。血清葡萄糖和甘油三酸酯水平也降低了，补充LCA和DCA可以逆转这些降低的趋势。定量蛋白质组学研究表明，在肝纤维化患者中，参与糖原代谢，胆固醇，胆汁酸生物合成和药物代谢的蛋白质（Cyp2b10，Cyp3a25和Cyp51a1）的表达水平发生了改变，而这些改变可通过补充LCA和DCA来逆转。这些结果表明，产生次级胆汁酸的细菌有助于宿主体内葡萄糖和甘油三酸酯水平的稳态和药物代谢，并且具有作为治疗代谢疾病的治疗靶标的潜力。