Journal of visualized experiments : JoVESep 17, 2026

Nerve damage linked to diabetes may cause digestive problems

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Sep 18, 2026

Abstract

Diabetes mellitus is frequently accompanied by gastrointestinal symptoms that may not be fully explained by autonomic neuropathy.

Gastrointestinal symptoms in diabetes can arise from specific injuries to the enteric nervous system and its cellular environment.
Human studies reveal gastric changes in interstitial cells of Cajal and colonic enteric neuronal loss linked to oxidative stress.
Dysmotility is most directly associated with myenteric injury, while submucosal injury could affect secretion and local immune control.
Current treatments primarily address symptoms rather than underlying causes.
Investigational therapies include heme oxygenase-1, interleukin-10, and microbiota-derived butyrate, but none are yet established.

Simplified

Diabetes mellitus is frequently accompanied by gastrointestinal symptoms, but these symptoms are not fully explained by extrinsic autonomic neuropathy and should not be equated with a single enteric lesion. Human biopsy and motility studies, complemented by experimental models, indicate that the enteric nervous system (ENS) and its neuromuscular niche can be injured in segment- and cell-specific ways. Human evidence supports gastric changes in interstitial cells of Cajal (ICC) and macrophages, and colonic enteric neuronal loss associated with oxidative stress; plexus-resolved and repair mechanisms are derived mainly from animal or in vitro studies. Recurrently implicated pathways include redox imbalance, immune remodeling, impaired glial cell line-derived neurotrophic factor (GDNF)-phosphoinositide 3-kinase (PI3K)/Akt signaling, enteric glial stress, and microbiota-metabolite signaling. Myenteric injury is most directly linked to dysmotility, whereas submucosal injury may alter secretion, barrier function, and local neuroimmune control. Current care remains symptom-directed. Heme oxygenase-1, interleukin-10, neurotrophic rescue, nicotinamide riboside, 5-hydroxytryptamine 4 receptor agonism, microbiota-derived butyrate, and extracellular vesicles are investigational rather than established disease-modifying therapies. Segment-specific biomarkers and human translational models are needed to connect cellular injury with symptoms and treatment response.

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Nerve damage linked to diabetes may cause digestive problems

Abstract

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