Diabetic gastrointestinal autonomic neuropathy: Integrating neuronal degeneration and gut microbial dysbiosis.

Abstract

Diabetic gastrointestinal autonomic neuropathy (DGAN) is a common and debilitating complication of diabetes, characterized by autonomic dysfunction in the gastrointestinal system. The complex pathophysiology of DGAN involves neuronal injury that is intrinsically linked to gut dysbiosis. Multiple factors, including hyperglycemia, oxidative stress, and inflammation, significantly contribute to neuronal damage, manifesting as symptoms such as delayed gastric emptying, diarrhea, and constipation. Recent studies have demonstrated that patients with diabetes experience substantial alterations in gut microbiota composition, potentially exacerbating gastrointestinal symptoms. Microbial metabolites may modulate neurotransmitter synthesis and release, directly affecting autonomic nerve function, while dysbiosis amplifies oxidative stress and inflammation, further compromising the enteric nervous system and worsening DGAN. Advances in multi-omics technologies now provide deeper insights into molecular mechanisms of DGAN and its interactions with microbiota. Early diagnosis leveraging biomarkers, gut microbiota analysis, and advanced imaging promises more effective interventions. Emerging therapeutic strategies targeting oxidative stress, inflammation, and gut microbiota represent promising approaches for managing DGAN. Future research should focus on large-scale, multi-ethnic studies and therapies targeting specific microbial metabolites to refine diagnosis and treatment approaches.