Intestinal adaptation: factors that influence morphology.
The lining of the intestinal tract is constantly renewed in a brisk but orderly fashion. Further acceleration of cell renewal is elicited by various stimuli, notably surgical shortening of the intestine and hyperphagia, which lead to prompt but persistent increases in mucosal mass. Progressive hypoplasia ensues when the small and large bowel are deprived of their normal contents, either by fasting (with or without parenteral nutrition) or by exclusion from intestinal continuity. All atrophic changes are reversed by refeeding or restoration of the normal anatomical disposition. Intestine responds to mucosal damage by regeneration from the crypts. Pancreatobiliary secretions mediate some of the tropic effects of chyme; systemic influences, both neurovascular and humoral, also play a part in the adaptive response of the gut.
D000222:Adaptation, Physiological; D000328:Adult; D000818:Animals; D002455:Cell Division; D003082:Colectomy; D003125:Colostomy; D005260:Female; D005755:Gastrins / Q000502:physiology; D004763:Glucagon-Like Peptides / Q000502:physiology; D006801:Humans; D006963:Hyperphagia / Q000473:pathology; D006965:Hyperplasia; D006984:Hypertrophy; D007082:Ileum / Q000601:surgery; D007410:Intestinal Diseases / Q000473:pathology; D007413:Intestinal Mucosa / Q000473:pathology; D007422:Intestines / Q000473:pathology* / Q000503:physiopathology / Q000601:surgery; D007583:Jejunum / Q000601:surgery; D009765:Obesity / Q000628:therapy; D010288:Parenteral Nutrition; D051381:Rats; D013217:Starvation / Q000473:pathology
D005755:Gastrins; D004763:Glucagon-Like Peptides