gastrins and Pancreatic-Diseases

Topics: Adenoma; Carcinoid Tumor; Endocrine System Diseases; Gastrins; Gastrointestinal Diseases; Glucagonoma; Histocytochemistry; Humans; Hyperinsulinism; Immunochemistry; Insulinoma; Islets of Langerhans; Pancreatic Diseases; Pancreatic Neoplasms; Peptic Ulcer; Somatostatinoma; Stomach; Vipoma

Topics: Animals; Cattle; Cholecystokinin; Dogs; Enteral Nutrition; Epidermal Growth Factor; Gastrins; Hormones; Humans; Insulin; Intestine, Small; Pancreas; Pancreatic Diseases; Pancreatic Polypeptide; Parasympathomimetics; Pituitary Gland; Rats; Secretin; Trypsin Inhibitors

Regulation of pancreatic exocrine secretion is comprised of a complex interplay between hormonal and nervous mechanisms. Stimulatory gut hormones which act via the circulation include secretin, CCK, gastrin and bombesin, while VIP operates through peptidergic nervous release. Pancreatic polypeptide and glucagon are two examples of circulating inhibitory hormones while inhibition by somatostatin is through a paracrine release mechanism. Although the effects of vagal cholinergic nerves have been previously thought to be indirect through hormone release evidence is now accumulating for a direct role. Altered hormone release has been noted in chronic pancreatic insufficiency, cystic fibrosis and coeliac disease and may contribute in an important way to the pathophysiology of these malabsorptive disorders.

Topics: Autonomic Nervous System; Bombesin; Cholecystokinin; Enkephalins; Gastrins; Gastrointestinal Hormones; Humans; Neurotensin; Pancreas; Pancreatic Diseases; Pancreatic Polypeptide; Secretin; Somatostatin; Vagus Nerve; Vasoactive Intestinal Peptide

Topics: Animals; Bombesin; Cholecystokinin; Endorphins; Gastrins; Hormones; Humans; Islets of Langerhans; Nerve Tissue Proteins; Neurons; Neurotensin; Pancreatic Diseases; Reflex; Somatostatin; Vasoactive Intestinal Peptide

Topics: Cholecystokinin; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Diseases; Gastrointestinal Hormones; Humans; Pancreatic Diseases; Secretin; Vasoactive Intestinal Peptide

Topics: Animals; Cholecystokinin; Dogs; Gastric Inhibitory Polypeptide; Gastric Juice; Gastrins; Gastrointestinal Hormones; Humans; Pancreatic Diseases; Radioimmunoassay; Secretin; Syndrome; Vasoactive Intestinal Peptide; Zollinger-Ellison Syndrome

Topics: Animals; Bicarbonates; Chemoreceptor Cells; Cholecystokinin; Digestion; Food; Gastrins; Humans; Intestinal Mucosa; Pancreas; Pancreatic Diseases; Pancreatic Hormones; Pancreatic Juice; Secretin; Sensory Receptor Cells

Tumoral secretions and pathophysiology of diarrhea were studied in 1 patient with pancreatic cholera. High concentrations of vasoactive intestinal peptide were found in both systemic blood and tumoral extracts, together with increased plasma levels of calcitonin and protaglandins E and Falpha. Gastric inhibitory peptide and gastrointestinal and pancreatic hormones were absent from the tumor, except for small amounts of glucagon, and their blood levels were normal. Decreased basal but normal pentagastrin-stimulated gastric acid secretion, normal basal and secretin-stimulated pancreatic secretion, increased volume of gallbladder bile with high bicarbonate, and low bile salt concentrations were observed, but the electrolyte content and flow rate of fluid passing the duodenojejunal junction were within normal limits. Small intestine was found to be the origin of the water and electrolyte fasting losses. Jejunum was the site of bicarbonate secretion. Jejunal glucose and leucine-stimulated water and sodium transports were also strikingly decreased, whereas the absorption rates of the sugar and amino acid were normal. Colon reabsorbed high amounts of water and sodium but increased potassium losses. Biological effects of vasoactive intestinal peptide may explain most of the patient's upper digestive secretion abnormalities and small intestinal function impairments, whereas secondary aldosteronism might explain the modified colonic function.

Topics: Adult; Bile; Blood Vessels; Calcitonin; Cholecystokinin; Cholera; Colon; Depression, Chemical; Diarrhea; Duodenum; Feces; Female; Gastric Mucosa; Gastrins; Glucagon; Humans; Ileostomy; Insulin; Insulin Secretion; Intestinal Secretions; Intestine, Small; Pancreas; Pancreatic Diseases; Pancreatic Neoplasms; Peptides; Prostaglandins E; Prostaglandins F; Secretin; Stomach

Topics: Digestion; Enzyme Therapy; Fats; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Gastrointestinal Hormones; Humans; Methods; Pancreas; Pancreatectomy; Pancreatic Diseases; Pancreatic Juice; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Animals; Dogs; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Intestine, Small; Liver; Liver Diseases; Pancreas; Pancreatic Diseases; Pentagastrin; Portal System; Rats; Secretory Rate

Topics: Biliary Tract Diseases; Ceruletide; Cholangiography; Cholelithiasis; Duodenal Ulcer; Endoscopy; Gastrins; Gastrointestinal Diseases; Gastrointestinal Hemorrhage; Gastrointestinal Hormones; Humans; Intestinal Absorption; Lactose Intolerance; Pancreatic Diseases; Peptic Ulcer; Radionuclide Imaging; Secretin; Stomach Neoplasms

Topics: Acute Disease; Adenoma, Islet Cell; Cholecystokinin; Chronic Disease; Gastrins; Humans; Methods; Pancreas; Pancreas Transplantation; Pancreatic Diseases; Pancreatic Neoplasms; Pancreatitis; Radiography; Secretin; Transplantation, Homologous; Zollinger-Ellison Syndrome

Topics: Air; Anemia, Pernicious; Angiography; Barium; Biopsy; Cholangiography; Colonic Diseases; Contrast Media; Cytodiagnosis; Duodenal Diseases; Endoscopy; Enema; Esophageal Diseases; Gastrins; Gastroenterology; Gastrointestinal Diseases; Gastrointestinal Neoplasms; Gastroscopy; Glucose; Glucuronidase; Gold Isotopes; Insulin; Liver Diseases; Methionine; Pancreatic Diseases; Peptic Ulcer; Peptides; Rectal Neoplasms; Rose Bengal; Selenium; Silicones; Stomach Neoplasms; Vagotomy

Topics: Acetamides; Acetylcholine; Amino Acids; Animals; Antibodies; Bicarbonates; Chemistry Techniques, Analytical; Cholecystokinin; Digestive System; Dogs; Duodenal Ulcer; Enzymes; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Humans; Pancreas; Pancreatic Diseases; Pancreatic Juice; Peptides; Secretin; Sheep; Stimulation, Chemical; Swine

Topics: Anemia, Pernicious; Antibodies; Aspirin; Feces; Galactosidases; gamma-Globulins; Gastric Juice; Gastrins; Gastrointestinal Diseases; Glutaminase; Humans; Intestinal Absorption; Intestinal Diseases; Intestines; Metabolism, Inborn Errors; Pancreatic Diseases; Pancreatitis; Radiography; Radionuclide Imaging; Triglycerides

Long-term use of proton pump inhibitors (PPIs) has been reported to worsen corpus atrophic gastritis in patients with Helicobacter pylori infection. On the other hand, PPIs have been associated with fundic gland-type gastric polyps and various histological changes. In the present study, we attempted to establish a protocol for omeprazole (OPZ) administration to rats over a longer period and examined the morphological changes in the gastric mucosa after administration of OPZ for 6 months. A total of 34 Wistar rats (8 weeks old) were used. In a preliminary experiment to determine the appropriate dose of OPZ, the rats had ad libitum access to food containing different doses of OPZ for 1 month. We found an approximate dose of 100 mg/kg body weight/day of OPZ to be most suitable from the point of view of intragastric pH, body weight, and serum gastrin level. In the experiment proper, rats were divided into two groups, either control or OPZ diets, and morphological changes in the gastric mucosa in each group were then examined by hematoxylin and eosin and immunohistochemical staining with alpha-amylase, trypsin, and chromogranin A. Multiple vacuolar degeneration of parietal cells and numerous small mucous cells were evident at 1 month after treatment with OPZ. At 6 months after treatment with OPZ, cystic degeneration and acinar-cell-like cells containing red granules positive for alpha-amylase and trypsin and negative for chromogranin A were detected in the OPZ rats. The serum gastrin level in the OPZ group was significantly higher than that in the control group. We have established a protocol for long-term administration of OPZ in rats that is a useful model for analyzing morphological changes after long-term PPI therapy. Long-term OPZ treatment causes hypergastrinemia and pancreatic acinar cell metaplasia in this animal model.

Topics: alpha-Amylases; Animals; Anti-Ulcer Agents; Body Weight; Chromogranin A; Dose-Response Relationship, Drug; Drug Administration Schedule; Gastric Acid; Gastric Acidity Determination; Gastric Mucosa; Gastrins; H(+)-K(+)-Exchanging ATPase; Male; Metaplasia; Models, Animal; Omeprazole; Pancreas; Pancreatic Diseases; Parietal Cells, Gastric; Proton Pump Inhibitors; Rats; Rats, Wistar; Time Factors; Trypsin

Topics: Adult; Carcinoid Tumor; Gastrins; Humans; Male; Neoplasms, Multiple Primary; Pancreatic Diseases; Stomach Neoplasms

Adult nesidioblastosis remains an uncommon and poorly understood condition creating both diagnostic and therapeutic dilemmas for clinicians. Despite the totipotent nature of hyperplastic pancreatic cells, nearly all accounts of nesidioblastosis described patients with symptoms of hypoglycemia. We herein describe two unique patients with adult nesidioblastosis with gastrin and pancreatic polypeptide secretion. Surgical resection rendered these two patients free of disease.

Topics: Aged; Duodenum; Gastrins; Humans; Male; Middle Aged; Pancreatectomy; Pancreatic Diseases; Pancreatic Polypeptide

This study was conducted to determine the effects of nicotine inhalation on the onset, progression, and sequential development of pancreatic lesions. Male Sprague-Dawley rats in groups of five were exposed to saline or nicotine aerosol twice daily for 15, 30, 45, and 60 min for 21 days. After sacrifice, blood samples were analyzed for plasma levels of nicotine, glucose, gastrin, and cholecystokinin. Pancreatic tissues were examined for pathological lesions. While there were no significant differences in plasma levels of glucose, gastrin, and cholecystokinin in all groups, there was a steady increase in plasma levels of nicotine with increased exposures to nicotine. Histopathological examination of pancreatic tissue revealed definitive pancreatic injuries that also appeared to be directly correlated with increased duration of nicotine exposure. The pathological changes of the pancreas were confined only to acinar cells of the exocrine pancreas. Two main types of cellular changes were observed: cellular swelling/vacuolation and nuclear condensation/cellular pyknosis. Both of these changes indicated tissue injuries in the pancreas. Transformation of the glandular acini to solid masses of epithelial cells was also observed. The results from our present study strongly suggest that the exocrine pancreas is very sensitive and susceptible to nicotine toxicity. Our data further indicate that early morphological changes in the pancreas induced by nicotine may occur without functional or metabolic alterations; however, such changes could occur at a later stage, when tissue and cellular changes become more extensive.

Topics: Administration, Inhalation; Animals; Blood Glucose; Cell Nucleus; Cholecystokinin; Cytoplasm; Gastrins; Male; Nicotine; Pancreas; Pancreatic Diseases; Rats; Rats, Sprague-Dawley; Vacuoles

Plasma gastrin and cholecystokinin (CCK) responses were measured after a pancreatoduodenectomy (PD) using the Billroth-I type reconstruction combined with distal partial gastrectomy (standard PD) and combined with preservation of the pylorus and the duodenal bulb (PPPD). Six unoperated patients, 4 men and 2 women, were studied as control subjects. Basal plasma levels of gastrin were significantly higher in controls than in patients who had a standard PD (p less than 0.05) and gastrin responses to a meal were also blunted in these patients. In contrast basal and postprandial levels of gastrin after PPPD were significantly higher than these found in patients with standard PD (p less than 0.05). Postprandial gastrin response after PPPD were similar in pattern to these found in controls. Integrated gastrin release after PPPD was less than that of the control but was significantly greater than that in patients with standard PD. Basal plasma levels of CCK in the patients after the standard PD were significantly lower than in controls and significantly higher postprandial levels of CCK were found after PPPD compared to standard PD (p less than 0.05). However integrated CCK from 0 to 120 minutes were not significantly different between PPPD and standard PD groups. Based on these observations concerning hormonal release of gastrin and CCK, preservation of the stomach and the duodenal bulb appears to be a more physiologic reconstructive procedure than the standard PD. In addition the operation probably has more beneficial effect on the injured pancreas in time.

Topics: Adolescent; Adult; Aged; Cholecystokinin; Eating; Female; Follow-Up Studies; Gastrectomy; Gastrins; Humans; Male; Middle Aged; Pancreatic Diseases; Pancreaticojejunostomy; Postoperative Period; Pylorus; Radioimmunoassay; Radionuclide Imaging

Topics: Adult; Duodenal Ulcer; Gastrins; Humans; Hyperinsulinism; Hypoglycemia; Insulin; Insulin Secretion; Male; Pancreatic Diseases; Vagotomy

The endocrine pancreas from four hypergastrinemic patients with recurrent peptic ulceration has been studied by light and electron microscopy. Greatly increased numbers of ducts and centroacinar cells have been observed associated with a striking increase in the number of islets and endocrine cells scattered in the acinar tissue (nesidioblastosis). The islet cells scattered throughout the exocrine parenchyma are of all the known islet cell types, with a prevalence of B and especially A cells. Many islets, probably formed de novo, are of a considerable size, have irregular contours and are in close apposition to centroacinar cells and ducts. The degree of nesidioblastosis and islet hyperplasia does not seem to be related to the plasma gastrin levels. Cytological changes have also been found in the islet cells of the hypergastrinemic patients compared with controls. These changes mainly affect the B cells and consist of a striking decrease in the number of mature secretory granules associated with a fairly extended ergastoplasm and Golgi apparatus and with a relevant increase in the number of immature granules. In two of the four patients examined, who had more severe hypergastrinemia, cytological signs of enhanced secretion are also recognized in A cells. The features indicating hypersecretion of B and A cells seem to be related to the plasma gastrin levels. The above findings indicate that chronic endogenous hypergastrinemia promotes proliferation and differentiation of islet cells and stimulates the secretory function of B cells and, to a lesser extent, of A cells, thus providing evidence for a trophic and secretagogue action of gastrin on the endocrine pancreas.

Topics: Female; Gastrins; Humans; Islets of Langerhans; Male; Microscopy, Electron; Middle Aged; Pancreatic Diseases; Peptic Ulcer

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)

Topics: Acarbose; Adaptation, Physiological; alpha-Glucosidases; Animals; Atrophy; Cholecystokinin; Copper; Diet; Digestive System Diseases; DNA; Gastric Inhibitory Polypeptide; Gastrins; Glucosidases; Glycoside Hydrolase Inhibitors; Insulin; Intestinal Absorption; Intestine, Small; Male; Oligosaccharides; Pancreatic Diseases; Penicillamine; Proteins; Rats; Rats, Inbred Strains; Sucrase; Trisaccharides

The results suggest that in the pancreatic atrophy the interrelations of gastrointestinal hormones are changed. These changes may be involved in the maintenance of the relatively high hormonal responses to feeding in the pancreatic atrophy.

Topics: Animals; Atrophy; Dogs; Eating; Gastrins; Gastrointestinal Hormones; Motilin; Pancreatic Diseases; Pancreatic Polypeptide

One-hour postprandial responses of plasma concentrations of pancreatic polypeptide, gastrin and motilin were measured in 4 dogs during 31 months of pancreatic atrophy development, produced by obstructing their pancreatic juice flow. Basal pancreatic polypeptide and gastrin concentrations decreased, while motilin concentration did not. During this period the animals displayed a significant postprandial response. These findings suggest that hormonal mechanisms involved in the digestive process are maintained in the period of the sharp disturbance of the pancreatic exocrine function.

Topics: Amylases; Animals; Atrophy; Bicarbonates; Dogs; Gastrins; Gastrointestinal Hormones; Motilin; Pancreatic Diseases; Pancreatic Juice; Pancreatic Polypeptide; Peptide Hydrolases

Topics: Animals; Atrophy; Diet; Digestion; Dogs; Gastrins; Gastrointestinal Hormones; Insulin; Meat; Motilin; Pancreatic Diseases; Pancreatic Polypeptide

Topics: Animals; Atrophy; Dogs; Food; Gastrins; Gastrointestinal Hormones; Motilin; Pancreatic Diseases; Pancreatic Polypeptide; Time Factors

Fasting and postprandial concentrations of pancreatic polypeptide, gastrin and motilin were measured during 2hrs after meat feeding. The byphasic rise of pancreatic polypeptide concentration occurred in 15 and 120 min and increase of gastrin concentration--in 15 min after feeding. Increase of motilin concentration occurred during the second hour. These findings complete our previous data and suggest that hormonal mechanisms involved in postprandial response are maintained even in pancreatic atrophy.

Topics: Animals; Atrophy; Digestion; Dogs; Gastrins; Gastrointestinal Hormones; Meat; Motilin; Pancreatic Diseases; Pancreatic Polypeptide; Time Factors

One hour postprandial responses of plasma concentrations of pancreatic polypeptide, gastrin and motilin were detected in healthy dogs. Pancreatic atrophy was produced in these animals by obstructing their pancreatic juice flow. Basal hormone concentrations in four animals did not change significantly during 11 months of pancreatic atrophy. During this period the animals displayed a significant postprandial response. These preliminary results suggest that hormonal mechanisms involved in the digestive process are maintained during pancreatic atrophy.

Topics: Amylases; Animals; Atrophy; Bicarbonates; Dogs; Fasting; Gastrins; Gastrointestinal Hormones; Motilin; Pancreas; Pancreatic Diseases; Pancreatic Juice; Pancreatic Polypeptide; Peptide Hydrolases

Relationships between hormonal secretions from the GI tract and gastric functional and/or pathological abnormalities could be studied according to 2 main lines : 1) gastric secretory changes could be the main symptom of hormonal secretory tumors, i.e. acid hypersecretion in the Zollinger Ellison syndrome, acid hyposecretion in pancreatic cholera and in somatostatinoma. In these cases, hormonal hypersecretion is directly responsible for the functional disturbances and the related symptoms; 2) gastric pathological conditions are sometimes accompanied by changes in hormonal secretion, but the level of interdependence is variable : high blood gastrin is directly depending upon the atrophic gastritis in pernicious anemia; this mechanism was also suggested in case of gastric carcinoma. Concerning ulcer disease, numerous problems are unsolved in respect to blood gastrin (basal and stimulated) abnormalities, as well as somatostatin and GIP secretions.

Topics: Aged; Anemia, Pernicious; Cholera; Duodenal Ulcer; Gastric Inhibitory Polypeptide; Gastric Juice; Gastrins; Gastrointestinal Hormones; Gastrointestinal Neoplasms; Humans; Pancreatic Diseases; Pancreatic Neoplasms; Somatostatin; Stomach Diseases; Vasoactive Intestinal Peptide; Zollinger-Ellison Syndrome

Topics: Cholecystokinin; Gastrins; Humans; Pancreas; Pancreatic Diseases; Pancreatic Hormones; Pancreatic Neoplasms; Secretin

Topics: Animals; Cholecystokinin; Dietary Fats; Dose-Response Relationship, Drug; Duodenum; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Diseases; Gastrointestinal Hormones; Histamine; Humans; Pancreatic Diseases; Pancreatic Juice; Secretin

Topics: Adolescent; Adult; Age Factors; Child; Child, Preschool; Female; Gastrins; Humans; Liver Diseases; Male; Middle Aged; Pancreatic Diseases; Radioimmunoassay; Sex Factors

Topics: Cholecystokinin; Cholelithiasis; Duodenal Ulcer; Esophageal Achalasia; Gastrins; Gastritis; Gastrointestinal Hormones; Humans; Pancreatic Diseases; Peptic Ulcer; Secretin; Stomach Neoplasms; Stomach Ulcer

Topics: Cholecystokinin; Diarrhea; Gastric Juice; Gastrins; Humans; Hyperplasia; Pancreatic Diseases; Peptides; Stomach

Topics: Gastrins; Gastrointestinal Diseases; Humans; Kidney Diseases; Liver Diseases; Pancreatic Diseases; Stomach Diseases

Topics: Duodenal Ulcer; Gastrectomy; Gastrins; Humans; Hyperplasia; Islets of Langerhans; Male; Middle Aged; Pancreatectomy; Pancreatic Diseases; Vagotomy; Zollinger-Ellison Syndrome

The clinical data are presented of two women with profound metabolic upset from exceptional water and electrolyte losses in diarrhoea. One had an islet-cell adenoma of the pancreas and the other abnormal islets. Gastric and pancreatic function were abnormal in both, consistent with the subsequent demonstration of a pancreatic and choleretic secretagogue in the tumour tissue and pancreatic and gastric secretagogues in circulating blood (Cleator, Thomson, Sircus, and Coombes, 1970).

Topics: Adenoma, Islet Cell; Adult; Diarrhea; Female; Gastrins; Humans; Hypercalcemia; Hypokalemia; Hyponatremia; Islets of Langerhans; Pancreas; Pancreatic Diseases; Pancreatic Neoplasms; Peptides; Radionuclide Imaging; Water-Electrolyte Balance

Topics: Adenoma, Islet Cell; Diarrhea; Gastrins; Humans; Hypokalemia; Pancreas; Pancreatic Diseases; Pancreatic Neoplasms; Secretin; Zollinger-Ellison Syndrome

Topics: Adrenal Gland Neoplasms; Adult; Child; Gastrins; Glucagon; Glucose Tolerance Test; Humans; Insulin; Insulin Secretion; Islets of Langerhans; Multiple Endocrine Neoplasia; Pancreatic Diseases; Pancreatic Neoplasms; Parathyroid Neoplasms; Tolbutamide

Topics: Biliary Tract Diseases; Cholangiography; Cholecystokinin; Gastrins; Humans; Intestine, Small; Pancreatic Diseases; Secretin; Stomach Diseases

Topics: Biliary Tract Diseases; Biopsy; Diagnosis, Differential; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastrointestinal Diseases; Gastroscopes; Humans; Liver Diseases; Male; Methods; Pancreatic Diseases; Pancreatic Juice