cholecystokinin and Enteritis

The hormone cholecystokinin was discovered in 1928 because of its ability to induce gallbladder contraction. Since then, cholecystokinin has been shown to possess multiple functions in the gastrointestinal tract and brain. This review discusses several significant developments in cholecystokinin biology that show how it plays a role in gastrointestinal diseases, including control of appetite.. Cholecystokinin was shown to induce satiety by interacting through CCK-1 receptors located in specialized regions of the hindbrain. Cholecystokinin also inhibits expression of orexigenic peptides in the hypothalamus and prevents stimulation of specialized neurons by ghrelin. In the pancreas, cholecystokinin increased the proliferation of insulin-producing beta cells and reduced insulin-induced hyperphagia. Elevated cholecystokinin levels decreased appetite and reduced intestinal inflammation caused by parasites and bacterial toxins.. Understanding the mechanisms by which cholecystokinin regulates orexigenic pathways in the body may lead to strategies for controlling appetite-related disorders such as obesity and bulimia. The reduction of intestinal inflammation by dietary fats (by elevating cholecystokinin) suggests that the hormone plays an integrated role in regulating the ingestion and digestion of food that may be relevant to inflammatory diseases of the gastrointestinal tract.

Topics: Animals; Appetite Regulation; Cholecystokinin; Enteritis; Gastrointestinal Diseases; Ghrelin; Humans; Hypothalamus; Intracellular Signaling Peptides and Proteins; Neuropeptides; Orexins; Satiety Response

The aims of this study were: 1) to obtain an experimental model reproducing the characteristics of chronicity and spontaneous relapses found in inflammatory bowel disease (IBD) and 2) to correlate these changes with intestinal motility and bacteria translocation. For this purpose, two groups of Sprague-Dawley rats were used: a treated group that received two subcutaneous injections of indomethacin (7.5 mg/kg) 48 h apart and a control group that received saline. Blood leukocytes, TNF, and fecal parameters were monitored for 90 days after treatment. In treated rats, a cyclic oscillation of blood leukocytes and TNF concomitant with an inverse correlation of fecal output was observed. Treated rats were then selected either during their highest or lowest blood leukocyte values for motor activity and microbiological evaluation. Controls were obtained in age-matched rats. Rats with high leukocyte levels showed a decrease of motor activity. In contrast, animals with low leukocyte levels presented hypermotility. Bacterial overgrowth accompanied by bacterial translocation was found in the group with high leukocytes, whereas no differences were observed between the control and indomethacin groups during the lowest leukocyte phase. We obtained a model of IBD characterized by a chronic cyclic oscillation of intestinal motility, flora, and inflammatory blood parameters. During the high-leukocyte stage, motor activity decrease is related to bacterial translocation. This phase is followed by a reactive one characterized by hypermotility associated with a decrease in both bacterial growth and leukocytes. However, as in IBD, this reaction seems unable to prevent a return to relapse.

Topics: Acute Disease; Animals; Anti-Inflammatory Agents, Non-Steroidal; Bacteria; Bacterial Infections; Bacterial Translocation; Cholecystokinin; Chronic Disease; Enteritis; Enzyme Inhibitors; Gastrointestinal Motility; Indomethacin; Injections, Subcutaneous; Intestinal Diseases; Leukocyte Count; Male; Nitroarginine; Rats; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha

1. The aim of investigation was to establish and compare the reversibility of tolerance to the antitransit effects of morphine by three different procedures: (a) acute inflammation of the gut, (b) lorglumide a cholecystokininA (CCKA) receptor antagonist, or (c) MK-801, an N-methyl-D-aspartate (NMDA) receptor ion channel blocker. The type of interaction between morphine and lorglumide or MK-801 on the inhibition of gastrointestinal transit (GIT) in naive animals was also evaluated. 2. Male Swiss CD-1 mice were implanted with 75 mg of morphine base or placebo pellets. Gastrointestinal transit was assessed with a charcoal meal and results expressed as % inhibition of GIT. Inflammation was induced by the intragastric (p.o.) administration of croton oil (CO), while controls received castor oil (CA) or saline (SS). Morphine was administered by subcutaneous (s.c.) or intracerebroventricular (i.c.v.) injection, to naive and tolerant animals treated with CO, CA or SS. Dose-response curves for s.c. morphine were also performed in naive and tolerant mice receiving 5.2 or 7.4 nmol (s.c.) lorglumide or MK-801, respectively. 3. The ED50 values for inhibition of GIT by s.c. morphine were: 45.9 +/- 2.7 and 250.1 +/- 3.1 nmol in naive and tolerant animals, respectively, demonstrating a five fold decrease in the potency of morphine. In naive animals, inflammation (CO) decreased the ED50 of morphine three times (14.4 +/- 2.2 nmol). However, no tolerance to s.c. morphine (ED50 16.4 +/- 2.6 nmol) was manifested during intestinal inflammation. After i.c.v. administration, a similar degree of tolerance to morphine was observed (4.8 fold decrease in potency). Intestinal inflammation had no effect on the ED50 values of i.c.v. morphine in naive and tolerant animals, showing that reversal of tolerance is related to local mechanism/s. Mean values for intestinal pH were 6.9 +/- 0.04 and 6.2 +/- 0.04 in SS and CO treated mice, respectively. In addition, morphine was 74 times more potent by the i.c.v. than by the s.c. route (naive-SS). 4. Morphine and lorglumide interacted synergistically in naive animals; in addition, the administration of lorglumide reversed tolerance to s.c. morphine. No interaction (additivity) was observed in naive animals when morphine and MK-801 were administered in combination. However, the drug completely reversed tolerance to the antitransit effects of morphine. 5. The present investigation shows that acute inflammation of the gut reverses tolerance to the an

Topics: Acute Disease; Animals; Cholecystokinin; Dizocilpine Maleate; Drug Tolerance; Enteritis; Gastrointestinal Transit; Male; Mice; Morphine; Proglumide; Receptors, N-Methyl-D-Aspartate

Topics: Adolescent; Child; Cholecystitis; Cholecystokinin; Duodenal Diseases; Duodenal Ulcer; Enteritis; Humans; Pancreatic Diseases; Pancreatitis

Topics: Barium Sulfate; Celiac Disease; Cholecystokinin; Colectomy; Colitis, Ulcerative; Enteritis; Gastrointestinal Motility; Humans; Ileostomy; Intestinal Diseases; Intestine, Small; Radiography

Topics: Bicarbonates; Cholecystokinin; Enteritis; Gallbladder Diseases; Gastric Acidity Determination; Gastrins; Gastritis; Pancreas; Pancreatitis; Pyrazoles; Secretin; Stimulation, Chemical; Stomach Ulcer

Topics: Amyloidosis; Biochemical Phenomena; Biochemistry; Cholangitis; Cholecystitis; Cholecystokinin; Colonic Neoplasms; Drug Therapy; Duodenum; Electrophoresis; Enteritis; Gastritis; Hemosiderosis; Humans; Intestinal Secretions; Leucyl Aminopeptidase; Liver Cirrhosis; Liver Diseases; Melanoma; Mucous Membrane; Nephrosis; Pancreatitis