title: Repeated gastric distension alters food intake and neuroendocrine profiles in rats.
abstract: 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. To test the effects of repeated gastric distension (RGD) on neuroendocrine factors involved in energy homeostasis, a permanent intra-gastric balloon was implanted in rats, and briefly inflated daily for 4 weeks. Though body weights and daily food intakes remained equivalent in RGD and control rats, a significant delay in the onset of feeding was present during the first and second, but not the third and fourth weeks of inflations. Despite equivalent body weights and daily caloric consumption, RGD animals had significantly decreased leptin levels (p<0.05), and tended to have increased fasting arcuate NPY levels (p=0.08), which were suppressed more than control animals following food intake (control and RGD decreases from baseline were 184.95% and 257.42%, respectively). NPY expression in the nucleus of the solitary tract followed a similar pattern. These data demonstrate that the act of regularly distending the stomach can have effects on the regulation of energy balance that are independent from those related to caloric consumption, and may be related to disorders such as BN, BED, and certain types of obesity in which meal termination is impaired.
authors: Department of Psychological Sciences and Ingestive Behavior Research Center, Purdue University, West Lafayette, IN 47907, USA. shargrav@purdue.edu
authors: Sara L
authors: SL
authors: Hargrave
authors: Kimberly P
authors: KP
authors: Kinzig
mesh_terms: D000818:Animals; D001111:Arcuate Nucleus of Hypothalamus / Q000378:metabolism; D001835:Body Weight / Q000502:physiology; D002032:Bulimia / Q000503:physiopathology; D004435:Eating / Q000502:physiology*; D004734:Energy Metabolism / Q000502:physiology*; D005247:Feeding Behavior / Q000502:physiology; D015905:Gastric Balloon; D006963:Hyperphagia / Q000503:physiopathology; D020738:Leptin / Q000097:blood*; D008297:Male; D009478:Neuropeptide Y / Q000096:biosynthesis*; D011333:Pro-Opiomelanocortin / Q000096:biosynthesis*; D051381:Rats; D020318:Rats, Long-Evans; D017552:Solitary Nucleus / Q000378:metabolism; D013270:Stomach / Q000502:physiology*
chemical_list: D020738:Leptin; D009478:Neuropeptide Y; D011333:Pro-Opiomelanocortin