Differential Gastric Motility, Gut Hormone, and Appetite Changes Following A Mixed Meal in People With Obesity and Healthy Controls.

Introduction: Understanding meal-induced changes of gut hormones, gastric motility, and appetite is crucial for developing therapies for obesity. We investigated glucose-dependent insulinotropic peptide (GIP), glucagon-like peptide-1 (GLP-1), ghrelin, and motilin influences on gastric motility and appetite, to compare healthy individuals and people with obesity.

Methods: Subjects (healthy n = 41; obesity n = 32) consumed a 270-kcal meal and a wireless motility capsule. GIP, active GLP-1, acyl-ghrelin, and motilin were measured by electrochemiluminescence. MotiliGI and GIMS software were used for motility analysis, while visual analog scoring measured appetite.

Results: Gastric emptying was more rapid in people with obesity than in healthy individuals (p < 0.01). Gastric emptying time was negatively associated with motility index and hunger contractions (p < 0.01, p < 0.05) in healthy individuals, but not in individuals with obesity. In controls, gastric motility index correlated positively with acyl-ghrelin (p < 0.01) and motilin (p < 0.0001), and negatively with GIP (p < 0.05), but not aGLP-1. In people with obesity, no gut hormones correlated with the motility index. In both groups, GIP and aGLP-1 correlated with decreased hunger (p < 0.0001, p = 0.001) and (p < 0.0001, p < 0.05), along with increased satiety in controls (p < 0.0001, p = 0.001) and people with obesity (p = 0.049, p = 0.01). Acyl-ghrelin correlated positively with hunger (p < 0.0001) and negatively with satiety (p = 0.049) in controls, but not in obesity. Motilin was neither associated with hunger nor satiety.

Conclusion: In the gastric phase, people with obesity show rapid gastric emptying with altered hormone and motility meal responses. In healthy individuals, GIP promotes satiety, and ghrelin and motilin promote hunger through actions on motility. Like GIP, GLP-1 promotes satiety along with trending suppression of gastric motility.