Gut microbiota modulate distal symmetric polyneuropathy in patients with diabetes

公会 糖尿病 肠道菌群 促炎细胞因子 血糖性 丁酸盐 医学 多发性神经病 内科学 胃肠病学 免疫学 炎症 内分泌学 生物 发酵 栖息地 食品科学 生态学
作者
Junpeng Yang,Xueli Yang,Guojun Wu,Fenglian Huang,Xiaoyang Shi,Wei Wei,Yingchao Zhang,Haihui Zhang,Lina Cheng,Lu‐Gang Yu,Jing Shang,Yinghua Lv,Xiaobing Wang,Rui Zhai,Pan Li,Bota Cui,Yuanyuan Fang,Xinru Deng,Shasha Tang,Limin Wang
出处
期刊:Cell Metabolism [Cell Press]
卷期号:35 (9): 1548-1562.e7 被引量:40
标识
DOI:10.1016/j.cmet.2023.06.010
摘要

The pathogenic mechanisms underlying distal symmetric polyneuropathy (DSPN), a common neuropathy in patients with diabetes mellitus (DM), are not fully understood. Here, we discover that the gut microbiota from patients with DSPN can induce a phenotype exhibiting more severe peripheral neuropathy in db/db mice. In a randomized, double-blind, and placebo-controlled trial (ChiCTR1800017257), compared to 10 patients who received placebo, DSPN was significantly alleviated in the 22 patients who received fecal microbiota transplants from healthy donors, independent of glycemic control. The gut bacterial genomes that correlated with the Toronto Clinical Scoring System (TCSS) score were organized in two competing guilds. Increased guild 1, which had higher capacity in butyrate production, and decreased guild 2, which harbored more genes in synthetic pathway of endotoxin, were associated with improved gut barrier integrity and decreased proinflammatory cytokine levels. Moreover, matched enterotype between transplants and recipients showed better therapeutic efficacy with more enriched guild 1 and suppressed guild 2. Thus, changes in these two competing guilds may play a causative role in DSPN and have the potential for therapeutic targeting.
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