GASTROINTESTINAL MOTILITY IN OBESITY

Citation
O. Wisen et Pm. Hellstrom, GASTROINTESTINAL MOTILITY IN OBESITY, Journal of internal medicine, 237(4), 1995, pp. 411-418
Citations number
48
Categorie Soggetti
Medicine, General & Internal
ISSN journal
09546820
Volume
237
Issue
4
Year of publication
1995
Pages
411 - 418
Database
ISI
SICI code
0954-6820(1995)237:4<411:GMIO>2.0.ZU;2-K
Abstract
Gastrointestinal motility is closely linked to the rate at which nutri ents become systemically available. Regulation of gastric emptying rep resents the most important brake against delivery of nutrients to the intestine in excess of digestive and absorptive capacity. In man, gast ric emptying is slowed in proportion to the energy density of the meal , which will level out the rate of energy delivery to the duodenum. St udies suggest a more rapid gastric emptying in obesity, although the o pposite has been reported in some experimental settings, Moreover, gas tric volume is larger in obese individuals and appropriate satiety sig nals are not triggered in response to gastric distension, Postprandial intestinal transit time in obesity is similar to that in normal-weigh t subjects, however, despite this fact, intestinal absorption of nutri ents is more efficient in obesity. Several regulatory mechanisms for g astrointestinal motility, such as the autonomous and enteric nervous s ystems and gastrointestinal regulatory peptides, are also of importanc e for feeding behaviour and metabolism. Dysfunction of the autonomous nervous system has been observed, the sensitivity to cholecystokinin i s decreased in obesity, and plasma concentrations of somatostatin and neurotensin are lower than in normal-weight subjects. These changes in regulatory mechanisms favour rapid gastrointestinal transit of ingest ed nutrients and promote rapid intestinal absorption in obesity and de creased satiety in response to ingested food. It is presently not know n whether the observed changes in gastrointestinal motility in obesity represent a primary feature linked to the pathogenesis of such diseas e.