title: Adaptation of the small intestine to induced maldigestion in rats. Experimental pancreatic atrophy and acarbose feeding.
abstract: Intestinal adaptation has been studied in rats with pancreatic atrophy induced by feeding a copper-deficient diet and penicillamine and in rats with carbohydrate maldigestion induced by feeding of an alpha-glucosidase inhibitor (acarbose). Pancreatic atrophy led to a significant increase of weight, protein, and DNA content as well as specific activities and total amounts of the enzymes sucrase and maltase in the distal but not in the proximal part of the small intestine. Plasma levels of CCK and GIP were significantly higher in rats with pancreatic atrophy, whereas plasma levels of gastrin and insulin were lower. Tissue concentrations of gastrin in the antrum and GIP in duodenum and jejunum were unchanged. Duodenal CCK and jejunal substance P, somatostatin, and VIP and ileal substance P and somatostatin were significantly decreased in rats with acinar atrophy. Glucosidase inhibition by acarbose feeding led to weight increase of the small intestine and cecum. This was more marked when acarbose was fed together with a fiber-free diet. Under these conditions the protein and DNA content also increased significantly in both gut segments and maltase and sucrase content predominantly in the distal part. Insulin plasma concentration decreased significantly in the acarbose-fed groups, whereas GIP, gastrin, and CCK plasma concentrations remained unchanged. After fiber-rich diet tissue concentrations of gastrin in the antrum and insulin in the pancreas were significantly higher and GIP concentrations in the duodenum and jejunum significantly lower than after fiber-free diet. Acarbose increased the pancreatic insulin concentration only in the fiber-free group and did not influence gastrin and GIP concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
mesh_terms: D020909:Acarbose; D000222:Adaptation, Physiological; D000818:Animals; D001284:Atrophy / Q000139:chemically induced / Q000503:physiopathology; D002766:Cholecystokinin / Q000097:blood; D003300:Copper / Q000172:deficiency; D004247:DNA / Q000378:metabolism; D004032:Diet; D004066:Digestive System Diseases / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology*; D005749:Gastric Inhibitory Polypeptide / Q000097:blood; D005755:Gastrins / Q000097:blood; D005959:Glucosidases / Q000037:antagonists & inhibitors*; D065089:Glycoside Hydrolase Inhibitors; D007328:Insulin / Q000097:blood; D007408:Intestinal Absorption; D007421:Intestine, Small / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D009844:Oligosaccharides / Q000494:pharmacology*; D010182:Pancreatic Diseases / Q000139:chemically induced / Q000503:physiopathology; D010396:Penicillamine; D011506:Proteins / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013393:Sucrase / Q000378:metabolism; D014312:Trisaccharides / Q000494:pharmacology*; D000520:alpha-Glucosidases / Q000378:metabolism
chemical_list: D005755:Gastrins; D065089:Glycoside Hydrolase Inhibitors; D007328:Insulin; D009844:Oligosaccharides; D011506:Proteins; D014312:Trisaccharides; D005749:Gastric Inhibitory Polypeptide; D003300:Copper; D004247:DNA; D002766:Cholecystokinin; D005959:Glucosidases; D000520:alpha-Glucosidases; D013393:Sucrase; D010396:Penicillamine; D020909:Acarbose