郑州大学袁慧娟、上海交通大学张晨红与赵立平以及南京医科大学张发明研究组合作发现，肠道菌群调节糖尿病患者远端对称性多神经病变(DSPN)。相关论文发表在2023年7月13日出版的《细胞—代谢》杂志上。
他们发现来自DSPN患者的肠道微生物群可以诱导db/db小鼠表现出更严重的周围神经病变表型。在一项随机、双盲、安慰剂对照试验(ChiCTR1800017257)中，与10名接受安慰剂的患者相比，22名接受健康供体粪便菌群移植的患者的DSPN显著缓解，不依赖于血糖控制。与多伦多临床评分系统(TCSS)评分相关的肠道细菌基因组被组织在两个相互竞争的行会中。增加具有较高丁酸盐产生能力的功能群1和减少含有更多内毒素合成途径基因的功能群2，可以改善肠道屏障完整性和降低促炎细胞因子水平。
此外，移植肠型与受体肠型匹配的治疗效果更好，功能群1更富集，功能群2更抑制。因此，这两个相互竞争的功能群的变化可能在DSPN中起致病作用，并具有治疗靶向的潜力。
据了解，DSPN是糖尿病(DM)患者常见的神经病变，其发病机制尚不完全清楚。
附：英文原文
Title: Gut microbiota modulate distal symmetric polyneuropathy in patients with diabetes
Author: Junpeng Yang, Xueli Yang, Guojun Wu, Fenglian Huang, Xiaoyang Shi, Wei Wei, Yingchao Zhang, Haihui Zhang, Lina Cheng, Lu Yu, Jing Shang, Yinghua Lv, Xiaobing Wang, Rui Zhai, Pan Li, Bota Cui, Yuanyuan Fang, Xinru Deng, Shasha Tang, Limin Wang, Qian Yuan, Liping Zhao, Faming Zhang, Chenhong Zhang, Huijuan Yuan
Issue&Volume: 2023-07-13
Abstract: 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.
DOI: 10.1016/j.cmet.2023.06.010
Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(23)00220-6
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