oxyntomodulin and Hypertrophy

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.

Topics: Adaptation, Physiological; Adult; Animals; Cell Division; Colectomy; Colostomy; Female; Gastrins; Glucagon-Like Peptides; Humans; Hyperphagia; Hyperplasia; Hypertrophy; Ileum; Intestinal Diseases; Intestinal Mucosa; Intestines; Jejunum; Obesity; Parenteral Nutrition; Rats; Starvation

The effect of ileo-jejunal transposition (IJT) on the intestinal adaptation after total colectomy was investigated in 4 mongrel dogs. Hyperenteroglucagonemia was observed in the IJT with colectomy group, especially in postprandial state. Obvious hyperplastic changes were observed in all part of the small intestinal mucosa in the colectomy with IJT group. However, there were no significant differences in body weight changes between the colectomy with IJT group and the colectomy group. Postprandial plasma gastrin levels were lower in the colectomy with IJT group compared to the control. These results suggest that IJT causes hyperenteroglucagonemia and intestinal mucosal hypertrophy in colectomized dogs. Enteroglucagon may have an inhibitory effect on postprandial gastrin release.

Topics: Adaptation, Physiological; Animals; Body Weight; Colectomy; Dogs; Gastrins; Glucagon; Glucagon-Like Peptides; Hypertrophy; Ileum; Intestinal Mucosa; Intestines; Jejunum; Peptides

Topics: Gastrins; Gastrointestinal Hormones; Glucagon-Like Peptides; Humans; Hypertrophy; Infant; Infant, Newborn; Neurotensin; Pyloric Stenosis; Radioimmunoassay; Somatostatin

A number of human diseases with intestinal adaptation have been investigated, including acute infective diarrhoea, intestinal resection, jejuno-ileal bypass, coeliac disease, tropical sprue, chronic pancreatitis and cystic fibrosis. In all, the newly isolated hormone enteroglucagon appeared to be elevated in proportion to the degree of adaptation. In rats after gut resection and cold adaptation, enteroglucagon was also elevated and the degree of elevation correlated closely with the crypt cell production rate (CCPR). Chronic administration of somatostatin suppressed both enteroglucagon and CCPR, while bombesin stimulated both. A crude preparation of enteroglucagon was found to directly stimulate DNA synthesis in enterocyte cultures. It is thus concluded that, at present, the most likely candidate for the humoral component of intestinal adaptation is the hormonal peptide enteroglucagon.

Topics: Adaptation, Physiological; Adult; Animals; Cattle; Diarrhea; Gastrointestinal Hormones; Glucagon-Like Peptides; Humans; Hypertrophy; Infant; Inflammation; Intestinal Diseases; Intestinal Mucosa; Intestine, Small; Intestines; Mice; Motilin; Obesity; Rats