Your new experience awaits. Try the new design now and help us make it even better

SYSTEMATIC REVIEW article

Front. Nutr.

Sec. Nutrition and Metabolism

Volume 12 - 2025 | doi: 10.3389/fnut.2025.1668470

Effects of probiotic supplementation on islet β-cell function in subjects with glucose metabolism disorders: a meta-analysis

Provisionally accepted
Mengyue  XiangMengyue Xiang1Xingkang  SaiXingkang Sai1Zemin  TuoZemin Tuo1Jiwen  BianJiwen Bian2Peng  WangPeng Wang3Xinming  ZhangXinming Zhang4*
  • 1Department of General Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China
  • 2Department of Oncology, Qingdao Public Health Clinical Center, Qingdao, China
  • 3Department of General Practice, Weifang Hospital of Traditional Chinese Medicine, Weifang, China
  • 4Department of General Surgery, Qingdao Traditional Chinese Medicine Hospital (Qingdao Hiser Hospital Affiliated of Qingdao University), Qingdao, China

The final, formatted version of the article will be published soon.

Background: Islet β-cell dysfunction is central to the pathophysiology of glucose metabolism disorders. Probiotic supplementation has been shown to benefit glycemic control, but existing evidence on β-cell function remains inconclusive. This meta-analysis investigated the effects of probiotic supplementation on pancreatic islet β-cell function, as assessed by the homeostasis model assessment for β-cell function (HOMA-β), in individuals with impaired glucose metabolism. Methods: A systematic search of PubMed, Embase, Web of Science, and the Cochrane Library was conducted. We included randomized controlled trials (RCTs) comparing probiotics with placebo or no additional treatment in adults with abnormal glucose metabolism. Random-effects meta-analysis was performed, accounting for the potential influence of heterogeneity. Results: Twelve RCTs involving 907 participants were included. Compared with controls, probiotic supplementation significantly improved HOMA-β (mean difference [MD]: 3.04%, 95% CI: 0.23 to 5.86; p = 0.03; I² = 92%). However, the sensitivity analysis limited to studies with low risk of bias did not show that probiotics has a significant influence on HOMA-β in these participants (MD: -1.31%, 95% CI: -6.30 to 3.68, p = 0.61; I2 = 63%). Subgroup analysis showed a significant benefit in participants with baseline HbA1c ≥ 8.5% (MD: 7.05%, 95% CI: 5.85 to 8.24; I² = 0%), but not in those with HbA1c < 8.5% (MD: 0.19%, 95% CI: -1.09 to 1.46; I² = 37%; p for subgroup difference < 0.001). Meta-regression further confirmed that higher baseline HbA1c was positively associated with greater HOMA-β improvement (coefficient = 2.91; p = 0.04; adjusted R² = 62.5%). Other factors, such as mean age, sex, baseline body mass index, HOMA-β, concurrent hypoglycemic treatment, or probiotic treatment duration, did not significantly affect the results. Conclusion: Probiotics might enhance islet β-cell function in individuals with glucose metabolism disorders, particularly among those with elevated baseline HbA1c levels. However, large-scale high-quality RCTs are needed to validate our findings.

Keywords: Diabetes Mellitus, gestational diabetes mellitus, prediabetes, HOMA-β, Probiotics

Received: 18 Jul 2025; Accepted: 16 Sep 2025.

Copyright: © 2025 Xiang, Sai, Tuo, Bian, Wang and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Xinming Zhang, 13963910911@163.com

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.