Liu Ping, Jin Meiping, Hu Ping, Sun Weiqian, Tang Yuyan, Wu Jiajun, Zhang Dongliang, Yang Licai, He Haidong, Xu Xudong
Division of Nephrology, Minhang Hospital, Fudan University, Shanghai, China.
Curr Res Microb Sci. 2024 Nov 17;7:100315. doi: 10.1016/j.crmicr.2024.100315. eCollection 2024.
The intestinal microbiota comprises approximately 10-10 species of bacteria and plays a crucial role in host metabolism by facilitating various chemical reactions. Secondary bile acids (BAs) are key metabolites produced by gut microbiota.Initially synthesized by the liver, BA undergoes structural modifications through the activity of various intestinal microbiota enzymes, including eukaryotic, bacterial, and archaeal enzymes. These modified BA then activate specific receptors that regulate multiple metabolic pathways in the host, such as lipid and glucose metabolism, energy balance, inflammatory response, and cell proliferation and death. Recent attention has been given to intestinal flora disorders in diabetic kidney disease (DKD), where activation of BA receptors has shown promise in alleviating diabetic kidney damage by modulating renal lipid metabolism and mitochondrial production. Imbalances in the intestinal flora can influence the progression of DKD through the regulation of bile acid and its receptor pathways. This review aims to propose a mechanism involving the gut-BA-diabetes and nephropathy axes with the goal of optimizing new strategies for treating DKD.
肠道微生物群由大约10-10种细菌组成,通过促进各种化学反应在宿主代谢中发挥关键作用。次级胆汁酸(BAs)是肠道微生物群产生的关键代谢产物。胆汁酸最初由肝脏合成,通过各种肠道微生物群酶(包括真核、细菌和古细菌酶)的活性进行结构修饰。这些修饰后的胆汁酸随后激活特定受体,调节宿主中的多种代谢途径,如脂质和葡萄糖代谢、能量平衡、炎症反应以及细胞增殖和死亡。最近,糖尿病肾病(DKD)中的肠道菌群紊乱受到关注,其中胆汁酸受体的激活已显示出通过调节肾脏脂质代谢和线粒体产生来减轻糖尿病肾脏损伤的前景。肠道菌群失衡可通过调节胆汁酸及其受体途径影响DKD的进展。本综述旨在提出一种涉及肠道-胆汁酸-糖尿病和肾病轴的机制,以优化治疗DKD的新策略。