Gastrointestinal dysmotility and impaired gut peptide-satiety coupling in men with spinal cord injury.

Overeating associated with neurogenic obesity in chronic spinal cord injury (SCI) may reflect disruptions in gastrointestinal transit, satiety hormone responses, and appetite regulation. In this pilot study, 16 men with SCI (50 % tetraplegia) and 16 controls without SCI consumed standardized meals (195 g and 390 g) during 2 different laboratory visits. Gastrointestinal (GI) motility was measured using the SmartPill Wireless Motility Capsule during the first visit, while postprandial levels of GI peptides, glucose, insulin, and triglycerides were assessed during the second. Ratings of hunger and satiety were collected pre- and post-prandially in both visits. SCI participants exhibited GI dysmotility and exaggerated glycemic and lipemic excursions (all, p < 0.05) consistent with delayed GI transit. Associations between GI peptides and ratings of hunger and satiety were weaker in SCI, including attenuated ghrelin-hunger and GLP-1-fullness coupling (p < 0.05). Instead, fullness was more strongly associated with glucose in SCI (p < 0.05), indicating a potential shift toward glycemic cues in appetite regulation. The association between insulin and GLP-1 was stronger in SCI, consistent with a possible compensatory incretin signaling in response to impaired metabolic regulation. Together, these findings suggest disrupted gut-brain and metabolic signaling in SCI may impair appetite regulation, highlighting the need to further investigate gut-brain communication in relation to food intake.