Repeated gastric distension alters food intake and neuroendocrine profiles in rats.

The consumption of a large food bolus leads to stomach distension. Gastric distension potently signals the termination of a meal by stimulating gastric mechanoreceptors and activating neuroendocrine circuitry. The ability to terminate a meal is altered in disorders such as bulimia nervosa (BN), binge-eating disorder (BED) and certain subtypes of obesity in which large quantities of food are frequently ingested. When a large meal is consumed, the stomach is rapidly stretched. We modeled this rapid distension of the stomach in order to determine if the neuroendocrine abnormalities present in these disorders, including increased gastric capacit3y, leptin dysregulation, and alterations in neuropeptide Y (NPY), and proopiomelanocortin (POMC) expression, were influenced by the rapid stretch aspect of repeatedly consuming a large meal.