This observational study reveals reduced gastric mucosal innervation in obesity and suggests GMID may indicate diabetes remission.
Objective Obesity is a risk factor for dysregulated gastric function and peripheral nerve degeneration. This study aimed to investigate the impact of obesity on the structural pathology and morphometry of gastric mucosal innervation. Methods Sixty patients with obesity (30 with and 30 without type 2 diabetes) undergoing sleeve gastrectomy and 15 healthy controls were recruited. Gastric mucosal nerve terminals at the antrum were immunostained using protein gene product 9.5 and quantified using stereology‐based morphometry to determine gastric mucosal innervation density (GMID). Results Patients with obesity had lower GMID than control participants (464.0 ± 157.5 vs. 789.7 ± 188.9 mm/mm 3 , p < 0.001). There was a further reduction in GMID in patients with diabetes than in those without diabetes (406.8 ± 113.9 vs. 521.2 ± 175.3 mm/mm 3 , p < 0.001). GMID was significantly associated with BMI and glycemic parameters (fasting blood glucose, HbA1c) in multilinear regression analyses. One year post surgery, 19 patients achieving diabetes remission showed higher GMID compared to those without remission (444.8 ± 111.5 mm/mm 3 vs. 341.1 ± 88.1 mm/mm 3 , p = 0.012). GMID remained an independent predictor for diabetes remission in multivariable logistic regression analyses. Conclusions Gastric mucosal innervation was significantly reduced by the synergistic effects of obesity and diabetes. GMID could serve as a potential biomarker for predicting diabetes remission following bariatric surgery.
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Yang et al. (2025) studied this question.
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