Gut microbiota-enteric nervous system crosstalk drives diabetic GI dysfunction through GLP-1, ghrelin, and VIP pathways
Diabetic gastroenteropathy is driven by microbiota-ENS axis dysfunction involving GLP-1, ghrelin, VIP, and nitric oxide signaling, with probiotics, prebiotics, and FMT showing therapeutic potential through ENS repair.
Quick Facts
What This Study Found
DGE driven by ENS impairment (not just vagus). Microbiota-ENS axis: SCFAs, bile acids, tryptophan. Peptide mediators: GLP-1, ghrelin, VIP, acetylcholine, NO. Microbiome therapies (probiotics, prebiotics, FMT): repair ENS + alleviate DGE. >50% of diabetics have GI symptoms.
Key Numbers
How They Did This
Narrative review of microbiota-ENS interactions in diabetic gastroenteropathy with focus on neuropeptide mediators.
Why This Research Matters
Over half of diabetic patients have GI symptoms that worsen glucose control. Understanding the microbiota-ENS-peptide axis reveals new therapeutic targets beyond traditional motility drugs.
The Bigger Picture
This positions the gut microbiome as the upstream driver of diabetic GI dysfunction, with neuropeptides as the mediators. Microbiome therapies targeting peptide signaling could address a major source of diabetic morbidity.
What This Study Doesn't Tell Us
Narrative review. Most microbiome-ENS evidence is preclinical. FMT evidence in diabetic GI dysfunction is limited. Peptide mediator contributions not quantified.
Questions This Raises
- ?Could combining GLP-1 drugs with probiotics improve DGE more than either alone?
- ?Which specific microbiota species are most important for ENS maintenance?
- ?Does GLP-1 drug-induced GI slowing worsen or improve DGE?
Trust & Context
- Key Stat:
- Microbiota-ENS-peptide axis Diabetic GI dysfunction is driven by microbiome-enteric nervous system crosstalk through GLP-1, ghrelin, and VIP peptide signaling—opening microbiome-targeted therapies
- Evidence Grade:
- Narrative review synthesizing preclinical and early clinical evidence. Strong conceptual framework.
- Study Age:
- Published in 2025.
- Original Title:
- Microbiota and enteric nervous system crosstalk in diabetic gastroenteropathy: bridging mechanistic insights to microbiome-based therapies.
- Published In:
- Frontiers in cellular and infection microbiology, 15, 1603442 (2025)
- Authors:
- Tao, Wang, Yu, Yunfeng, Tan, Danni, Huang, Xiangning, Huang, Jiawang, Lin, Chuanquan, Yu, Rong
- Database ID:
- RPEP-13772
Evidence Hierarchy
Frequently Asked Questions
Why do diabetics have stomach problems?
Over half of diabetic patients have GI symptoms. This review explains it is because diabetes damages the gut's own nervous system (ENS) through changes in gut bacteria. The damaged ENS cannot properly control digestion, leading to nausea, bloating, and irregular bowel movements.
Could probiotics help diabetic stomach problems?
Emerging evidence suggests yes. By restoring healthy gut bacteria, probiotics and related therapies may repair the damaged enteric nervous system and improve GI symptoms through restored GLP-1, ghrelin, and VIP peptide signaling. This is a promising but early-stage approach.
Read More on RethinkPeptides
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Cite This Study
https://rethinkpeptides.com/research/RPEP-13772APA
Tao, Wang; Yu, Yunfeng; Tan, Danni; Huang, Xiangning; Huang, Jiawang; Lin, Chuanquan; Yu, Rong. (2025). Microbiota and enteric nervous system crosstalk in diabetic gastroenteropathy: bridging mechanistic insights to microbiome-based therapies.. Frontiers in cellular and infection microbiology, 15, 1603442. https://doi.org/10.3389/fcimb.2025.1603442
MLA
Tao, Wang, et al. "Microbiota and enteric nervous system crosstalk in diabetic gastroenteropathy: bridging mechanistic insights to microbiome-based therapies.." Frontiers in cellular and infection microbiology, 2025. https://doi.org/10.3389/fcimb.2025.1603442
RethinkPeptides
RethinkPeptides Research Database. "Microbiota and enteric nervous system crosstalk in diabetic ..." RPEP-13772. Retrieved from https://rethinkpeptides.com/research/tao-2025-microbiota-and-enteric-nervous
Access the Original Study
Study data sourced from PubMed, a service of the U.S. National Library of Medicine, National Institutes of Health.
This study breakdown was produced by the RethinkPeptides research team. We analyze and report published research findings without making health recommendations. All interpretations are based solely on the published abstract and study data.