Characteristic dysbiosis in patients with type 2 diabetes and hyperuricemia, and the effect of empagliflozin on gut microbiota.

IF 4.2 3区医学 Q1 ENDOCRINOLOGY & METABOLISM

World Journal of Diabetes Pub Date : 2025-04-15 DOI:10.4239/wjd.v16.i4.102970

Xin-Ru Deng, Yu-Jia Zhai, Xiao-Yang Shi, Sha-Sha Tang, Yuan-Yuan Fang, Hong-Yan Heng, Ling-Yun Zhao, Hui-Juan Yuan

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引用次数: 0

Abstract

Background: Gut microbiota play a crucial role in metabolic diseases, including type 2 diabetes (T2DM) and hyperuricemia (HUA). One-third of uric acid is excreted into the intestinal tract and further metabolized by gut microbiota. Thus, the gut microbiota might be a new therapeutic target for HUA. Empagliflozin significantly lowers serum uric acid levels and contributes to cardiovascular benefits which are partly attributed to altered gut microbiota. We hypothesize that gut dysbiosis in patients with diabetes and HUA, and the reduction of uric acid by empagliflozin, may be mediated by gut microbiota.

Aim: To investigate dysbiosis in patients with T2DM and HUA, and the effect of empagliflozin on gut microbiota associated with purine metabolism.

Methods: In this age and sex-matched, case-control study, we recruited 30 patients with T2DM and HUA; 30 with T2DM; and 30 healthy controls at the Henan Provincial People's Hospital between February 2019 and August 2023. Nine patients with T2DM and HUA were treated with empagliflozin for three months. Gut microbiota profiles were assessed using the 16S rRNA gene.

Results: Patients with T2DM and HUA had the highest total triglycerides (1.09 mmol/L in heathy control vs 1.56 mmol/L in T2DM vs 2.82 mmol/L in T2DM + HUA) and uric acid levels (302.50 μmol/L in heathy control vs 288.50 μmol/L in T2DM vs 466.50 μmol/L in T2DM + HUA) among the three groups. The composition of the gut microbiota differed significantly between patients with T2DM and HUA, and those with T2DM/healthy controls (P < 0.05). Notably, patients with T2DM and HUA demonstrated a deficiency of uric acid-degrading bacteria such as Romboutsia, Blautia, Clostridium sensu stricto 1 (P < 0.05). Empagliflozin treatment was associated with significantly reduced serum uric acid levels and purine metabolism-related pathways and genes in patients with T2DM and HUA (P < 0.05).

Conclusion: Gut dysbiosis may contribute to the pathogenesis of HUA in T2DM, and empagliflozin may partly restore the gut microbiota related to uric acid metabolism.

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2型糖尿病合并高尿酸血症患者的特征性生态失调及恩格列净对肠道菌群的影响

背景：肠道微生物群在代谢性疾病（包括2型糖尿病（T2DM）和高尿酸血症（HUA））中起着至关重要的作用。三分之一的尿酸排泄到肠道，并进一步被肠道菌群代谢。因此，肠道微生物群可能是HUA的一个新的治疗靶点。恩格列净显著降低血清尿酸水平，有助于心血管的益处，这部分归因于肠道微生物群的改变。我们假设糖尿病和HUA患者的肠道生态失调以及恩格列净对尿酸的降低可能是由肠道微生物群介导的。目的：探讨T2DM合并HUA患者的生态失调及恩格列净对嘌呤代谢相关肠道菌群的影响。方法：在这项年龄和性别匹配的病例对照研究中，我们招募了30例T2DM合并HUA患者；T2DM患者30例；2019年2月至2023年8月期间在河南省人民医院进行的30例健康对照。9例T2DM合并HUA患者用恩格列净治疗3个月。使用16S rRNA基因评估肠道微生物群。结果：T2DM合并HUA患者的总甘油三酯（健康对照组1.09 mmol/L， T2DM组1.56 mmol/L， T2DM + HUA组2.82 mmol/L）和尿酸水平（健康对照组302.50 μmol/L， T2DM组288.50 μmol/L， T2DM + HUA组466.50 μmol/L）在三组中最高。T2DM和HUA患者以及T2DM/健康对照组的肠道菌群组成差异显著（P < 0.05）。值得注意的是，T2DM和HUA患者尿酸降解菌如Romboutsia、Blautia、Clostridium sensu stricto 1缺乏（P < 0.05）。恩格列净治疗与T2DM合并HUA患者血清尿酸水平和嘌呤代谢相关通路及基因显著降低相关（P < 0.05）。结论：肠道生态失调可能参与T2DM HUA发病机制，恩格列净可部分恢复与尿酸代谢相关的肠道菌群。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

World Journal of Diabetes ENDOCRINOLOGY & METABOLISM-

自引率

2.40%

发文量

909

期刊介绍： The WJD is a high-quality, peer reviewed, open-access journal. The primary task of WJD is to rapidly publish high-quality original articles, reviews, editorials, and case reports in the field of diabetes. In order to promote productive academic communication, the peer review process for the WJD is transparent; to this end, all published manuscripts are accompanied by the anonymized reviewers’ comments as well as the authors’ responses. The primary aims of the WJD are to improve diagnostic, therapeutic and preventive modalities and the skills of clinicians and to guide clinical practice in diabetes. Scope: Diabetes Complications, Experimental Diabetes Mellitus, Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus, Diabetes, Gestational, Diabetic Angiopathies, Diabetic Cardiomyopathies, Diabetic Coma, Diabetic Ketoacidosis, Diabetic Nephropathies, Diabetic Neuropathies, Donohue Syndrome, Fetal Macrosomia, and Prediabetic State.