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At least 1,117 records · Page 62Linked to original sources
PubMed1997

Role of peptide YY in regulation of duodenal motility during the interdigestive period in sheep.

Temporal coordination between duodenal migrating myoelectric complexes (MMC) and pancreatic exocrine secretion, and the effects of porcine peptide YY (PYY) on gastroduodenal motility and pancreatic exocrine secretion were examined during the interdigestive period in conscious mature sheep. Fluid and enzyme secretions from the exocrine pancreas showed a periodic pattern corresponding to the phases of duodenal MMC, although these secretion rates were maintained at a high level during phase II in sheep. Intravenous continuous infusion of PYY at doses ranging from 50 to 200 pmol.kg-1.h-1 or intravenous bolus infusion of PYY at doses ranging from 50 to 200 pmol.kg-1 showed a tendency to prolong the first cycle of the duodenal MMC and significantly shorten the second cycle. However, there was almost no effect on ruminal contractions from the PYY administration. In the pancreatic exocrine secretion, PYY could inhibit only bicarbonate secretion at only the highest dose of 200 pmol.kg-1. These results imply that endogenous PYY may play a physiological role in the regulation of the duodenal MMC cycles in sheep but not in ruminal contractions. PYY seems unlikely to regulate the pancreatic exocrine secretion in normal sheep, because a supraphysiological dose of PYY was required to inhibit the pancreatic exocrine secretion.

Amylases↗
PubMed1998

Effects of vertebrate growth factors on digestive gland cells from the mollusc Pecten maximus L.: an in vitro study.

In relation with the digestive cycle, the digestive gland cells of bivalve molluscs undergo a sequence of cytological changes which is controlled by external and internal effectors such as putative gastrointestinal hormones and growth differentiation factors. A tissue dissociation method was developed to investigate the in vitro effect of the vertebrate growth and differentiation factors: insulin, insulin growth factor I (IGF-I), basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) on the digestive gland cells of the scallop Pecten maximus. All these vertebrate peptides induced a dose-dependent increased incorporation of 3H-leucine and 14C-uridine in whole digestive gland cell suspensions. However, after Percoll density gradient purification of the digestive cells, only stem and undifferentiated enriched cell fractions were responsive to the different peptides. In addition, insulin and IGF-I, but not EGF and bFGF, stimulated 3H-leucine incorporation in control dispersed mantle edge cells. These results suggest that insulin-related peptides could work as general growth promoting factors in molluscs. On the other hand, EGF and bFGF, or at least their molluscan counterparts, may be efficient growth differentiation factors in the regenerative processes occurring in the digestive gland of molluscs.

Animals↗
PubMed2004

Mixed acinar-endocrine carcinoma of the pancreas. A clinicopathological study and comparison with acinar-cell carcinoma.

We compared the clinicopathological features of acinar-cell carcinomas (ACCs) with those of mixed acinar-endocrine carcinomas (MAECs). Specimens from 37 patients with ACC and 6 patients with MAEC were examined histologically and immunohistochemically. The mean age of ACC and MAEC patients was similar (61.3 years versus 58.4 years), but the sex ratio differed (ACC, 29 males and 8 females; MAEC, 2 males and 4 females). The size of the tumor was large in both cases (ACC, 13.8 cm in diameter; MAEC, 8.2 cm). Immunohistochemically, more than half of the tumor cells in all tumors, whether ACC or MAEC, stained for trypsin. In 20 of the 37 ACCs (54%), scattered endocrine cells (SECs) were found, which stained positively for synaptophysin (SYN) and/or chromogranin A (CGA). Interestingly, there was also a difference in the sex ratio between ACC patients without SECs (16 males and 1 female) and ACC patients with SECs (13 males and 7 females). In MAECs, the cells staining for SYN were more common than those staining for CGA and made up more than one-third of the neoplastic-cell population. In all but one case (in which the endocrine component was arranged in islet-like cell clusters), the endocrine cells were intimately mixed with trypsin-positive tumor cells. The endocrine cells only rarely expressed one of the known pancreatic or gastrointestinal hormones. Both ACCs and MAECs had a high proliferation rate and lacked p53 overexpression or progesterone and estrogen receptors. This study revealed that ACCS and MAECs share most clinicopathological features and, therefore, may form a single tumor entity, though they differ in the number of endocrine cells. The frequent identification of endocrine cells in these tumors suggests the existence of a pluripotent cell of origin that is capable of differentiating into acinar and endocrine cells.

Adolescent↗
PubMed2006

Well-differentiated endocrine tumor of the distal common bile duct: a case study and literature review.

Primary carcinoid tumors of the extrahepatic biliary tree are exceedingly rare, accounting for 0.2-2% of all digestive carcinoids. The authors in this study describe a case of biliary duct primary well-differentiated endocrine tumor in a 30-year-old man with symptoms of biliary obstruction and watery diarrhoea. Abdominal ultrasound showed a 2-cm solid lesion in the head of the pancreas, compressing the distal common bile duct. A computed tomography scan confirmed these findings, revealing the hypervascular pattern of the tumor. Gastrointestinal hormonal screening demonstrated an increase in plasma serotonin. The patient underwent standard pylorus-preserving pancreatoduodenectomy. Pathological examination showed a neuroendocrine tumor of the distal common bile duct measuring 1.8 cm in greatest dimension. The tumor cells were immunopositive for neuron-specific enolase (NSE), chromogranin A, synaptophysin, serotonin, and cytokeratin. Stains for gastrin and somatostatin were negative. Seven years later, the patient is well, with no evidence of disease. Given the site of these tumors and the difficulty in differentiating them from periampullary lesions, decisions as to the appropriate surgical approach may be problematic. After an exhaustive review of the literature, the authors conclude that pancreatoduodenectomy is the treatment of choice.

Adult↗
PubMed2003

Gastric mucosal cell protection by epidermal growth factor in primary monolayer culture of guinea pig gastric mucous cells.

BACKGROUND: Epidermal growth factor (EGF) has an anti-ulcer effect, but the mechanisms of this gastric mucosal protection are incompletely understood. We have suggested the importance of mucin as a mucosal protectant. We investigated whether increased mucin biosynthesis might be involved in the gastric mucosal protection conferred by EGF. METHODS: EGF and then ethanol were added to primary monolayer cultures of guinea pig gastric mucous cells, in which factors such as gastric acid and gastrointestinal hormones were excluded. Mucin and prostaglandin E(2) (PGE(2)) were assayed. RESULTS: Cytoprotection induced by EGF was demonstrated. Mucin biosynthesis and PGE(2) release were both significantly increased by EGF. When endogenous PGE(2) synthesis was inhibited by pretreatment with 10(-5) M or 10(-4) M indomethacin (IND), mucin biosynthesis was still significantly increased by EGF. Ethanol-induced cell damage was concentration-dependent in cultures with no other additions (normal PGE(2) and mucin biosynthesis). Damage by ethanol was decreased by EGF pretreatment (increased PGE(2) and mucin biosynthesis). Damage by ethanol was increased by 10(-5) M IND pretreatment (decreased PGE(2); normal mucin biosynthesis) and by 10(-4) M IND pretreatment (decreased PGE(2) and mucin biosynthesis). Ethanol-induced damage was decreased by EGF pretreatment even in the presence of 10(-5) M and 10(-4) M IND (decreased PGE(2); increased mucin biosynthesis). CONCLUSIONS: Increased mucin biosynthesis, induced by EGF independently of PGE(2), protects gastric mucous cells.

Animals↗
PubMed2001

Recent findings in the study of postprandial lipemia.

The study of postprandial metabolism is in the early stages compared with other areas of atherosclerosis research. Recent advances in postprandial research have included improvements in methodology and the investigation of factors that modulate the lipemic response to a meal. Enough studies have now been performed that normal ranges have been identified for blood triacylglycerol (TAG) concentrations that occur after a healthy patient consumes a standardized-mixed meal or a high-fat shake designed to elicit lipemia. Typical postprandial concentrations of other metabolites, such as apolipoproteins B48 and B100 or gastrointestinal hormones (eg, cholecystokinin), have not been studied sufficiently to be able to qualify what represents a standard postprandial response. The method of data analysis is also a key point to consider. Data from children are now becoming available, and the specific effects of ethnicity have just begun to be explored. New areas of study include the effects of different fatty acids (monosaturates or polyunsaturates), the sources of chylomicron lipids (dietary TAG and cholesterol versus that newly synthesized in the body), and the effects of alcoholic beverages consumed with the meal. Variables that can also affect the results of a meal test are under investigation. These include the type of food that is consumed the day before the meal test, the time of day the test is performed, and the palatability of the food. Given solid evidence that delayed postprandial lipemia is an independent risk factor for coronary heart disease, future scientific investigation in the area of postprandial metabolism is likely to yield discoveries that will significantly contribute to advancements in disease treatment.

Digestion↗
PubMed1985

Prevention and treatment of infectious diarrhea. Speculations on the next 10 years.

The next decade should explode with exciting schemes and novel agents for the prevention and treatment of infectious diarrhea. The development of oral, nonabsorbed antibiotics will continue, but new antidiarrheal drugs, such as gastrointestinal hormone analogues and alpha-adrenergic agonists, will be added to our therapeutic armamentarium. Improved oral rehydration solutions, such as glycine in electrolyte solution, promise to revolutionize the management of diarrhea by diminishing diarrheal stool volume to the point where losses are too small to be clinically relevant. Infant formulas and adult oral solutions fortified with antibodies raised against selected enteropathogens may provide a way to prevent infectious diarrheas in infants and travelers. Advances in genetic engineering will usher in a new era of experimental and licensed enteric vaccines, including those against cholera, Escherichia coli, Shigella, typhoid fever, and rotavirus.

Animals↗
PubMed1987

Role of peptide radioimmunoassay in understanding peptide-peptide interactions and clinical expression of gastroenteropancreatic endocrine tumors.

Peptide radioimmunoassay has become an important clinical and research tool in understanding the role of peptides in the pathophysiology of gut endocrine tumor syndromes. A gut peptide radioimmunoassay laboratory has been established for the diagnosis and clinical monitoring of endocrine tumors of the gastroenteropancreatic (GEP) system. Radioimmunoassay has enhanced our awareness that co-occurring peptide interactions may modify and ultimately influence the clinical expression of these tumors. Furthermore, it has helped develop a rationale for the use of prototype peptides such as somatostatin and its long-acting analogue Sandostatin (SMS 201-995) in the management of GEP tumors. This group's experience, as well as the experience of other investigators, is presented, and the clinical utility of peptide radioimmunoassay in the field of gut endocrinology is demonstrated.

Adult↗
PubMed1981

Reduced tissue content of vasoactive intestinal peptide in aganglionic colon of Hirschsprung's disease.

The colonic tissue content of immunoreactive vasoactive intestinal peptide was measured in four children with histologically proven Hirschsprung's disease. The concentration of vasoactive intestinal peptide was lower in the aganglionic bowel than in nearby normal bowel. Similar results have been described for another gastrointestinal peptide: substance P. Abnormalities of peptidergic control may contribute to the motility disorder of congenital aganglionic colon.

Child↗
PubMed1992

Somatostatin stimulation of the normal esophagus.

The inhibitory effects of somatostatin on gastric and small bowel motor function are well documented. However, the effects of somatostatin on esophageal body motility and lower esophageal sphincter tone are not completely defined. We investigated the effects of octreotide, a long-acting somatostatin analogue, on the esophageal body and the lower esophageal sphincter in 15 healthy volunteers. Lower esophageal sphincter tone was increased by octreotide infusion. Esophageal body contraction amplitude and velocity were also increased by octreotide infusion. Our data show that somatostatin stimulates the normal human esophagus, an action mediated either by a direct effect, a central nervous system action, or the inhibition of the secretion of gastrointestinal hormones that influence esophageal motor activity.

Adult↗
PubMed1983

Primary amino acid sequence similarity between human epidermal growth factor-urogastrone, human pancreatic secretory trypsin inhibitor, and members of porcine secretin family.

Sequence similarities are detected between human epidermal growth factor-urogastrone, human pancreatic secretory trypsin inhibitor, and members of the secretin family of gastrointestinal hormones, particularly gastric inhibitory peptide. These similarities suggest a common evolutionary origin for these proteins and a possible functional relationship, as evidenced by the ability of human epidermal growth factor-urogastrone and human pancreatic secretory trypsin inhibitor to form a complex with protease and the ability of human epidermal growth factor-urogastrone and secretin family members to inhibit gastric acid secretion.

Amino Acid Sequence↗
PubMed1979

Localization and molecular heterogeneity of cholecystokinin in the central and peripheral nervous system.

Immunocytochemistry and radioimmunochemistry demonstrate the occurrence of the gastrointestinal hormone cholecystokinin (CCK) in both the central and peripheral nervous system of the guinea pig. CCK nerves are particularly numerous in the neocortex, the hippocampus, the amygdaloid nuclei, the hypothalamus, the spinal cord and in the colon. The nerves contain 5 molecular components of CCK, with gel chromatographical elution constants (Kav) of 0.05, 0.50, 0.90, 1.10 and 1.30, respectively. The four latter correspond to triacontatriapeptide CCK and its COOH-terminal dodeca-, octa- and tetrapeptide portions, respectively. Cholecystokinins are hence widely distributed in the nervous system and occur in the substantial quantities (greater than or equal to 0.2 nmol CCK-8-equiv./g) in several distinct regions.

Animals↗
PubMed1976

A reliable method for generating antibodies against pancreozymin, secretin and gastrin.

High specific antibodies against the gastrointestinal hormones pancreozymin, secretin, and gastrin were generated by coupling these peptides with N,N'-carbonyldiimidazole to bovine serum albumin. None of the antisera showed any cross reaction with gut and pancreatic hormones tested for cross reactivity. The dilution of antisera which were useful for the detection of 5-250 pg of hormone in human serum were 1:150 000 for secretin, 1:2000 for gastrin, and 1:2000 for pancreozymin. The N,N'-carbonyldiimidazole reagent is therefore highly effective for binding labile peptides to protein carriers without destroying the immunogenic features.

Antibody Formation↗
PubMed1975

Effect of prostaglandins E1, E2 and F2alpha and pentagrastin on the gall bladder pressure in dogs.

The effect of prostaglandins E1, E2 and F2alpha on the gall bladder pressure was studied in anesthetized dogs with and without clamping of the cystic duct. Both PGE1 and PGE2 lowered the gall bladder pressure when the initial pressure was higher than 5 mm Hg, but caused no significant change when the initial pressure was lower than 3 mm Hg. On the other hand, PGF2alpha increased the gall bladder pressure regardless of its initial pressure. When the cystic duct was clamped, PGF2alpha markedly increased the gall bladder pressure while both PGE1 and PGE2 increased it slightly. This observation suggests that the smooth muscle in the gall bladder is markedly stimulated by PGF2alpha and stimulated to a lesser degree by PGE1 or PGE2. Furthermore, PGF2alpha appears to constrict, and PGE1 or PGE2 appears to relax the sphincter of Oddi. Pretreatment with indomethacin did not affect or slightly potentiated the cholecystokinetic effect of the three prostaglandins but abolished that of pentagastrin, suggesting that prostaglandins are possible mediators for the cholecystokinetic action of the gastrointestinal hormones.

Animals↗
PubMed1979

Inhibition of gastric acid secretion by a glycoprotein isolated from human urine (human urinary gastric inhibitor).

The gastric antisecretory activity of an inhibitor newly isolated from human urine (Human Urinary Gastric Inhibitor or HUGI) has been studied. HUGI was given intravenously and its activity determined in the following test systems: gastric secretion in the rat with pyloric ligation; gastric secretion in the dog with a Heidenhain pouch stimulated with pentagastrin, histamine and a protein meal; acid secretion by the isolated gastric mucosa of the rat; gastrointestinal motility; bile flow and gall-bladder tone and arterial and venous blood pressure and heart rate. HUGI was found to have marked activity only in the pyloric-ligated rats and in the dogs with Heidenhain pouches stimulated by a protein meal. Particularly in the dog, HUGI (0.1 to 6.4 micrograms/kg, i.v) markedly inhibited gastric secretion, dose-dependently and without changing the plasma gastrin concentration. Negative results were obtained in the other tests, but these results serve to demonstrate that HUGI is an inhibitor well-differentiated from other glycoproteins or peptides with gastric antisecretory activity, such as urogastrone and GIP. The results obtained to date are not sufficient to allow the mechanism of action of HUGI to be defined.

Animals↗
PubMed1979

Effect of prostaglandin E1 and indomethacin on responses of longitudinal muscle of guinea-pig ileum to cholecystokinin.

The effect of prostaglandin E1 (PGE1) and indomethacin (IND) cholecystokinin (CCK)-induced contractions of guinea-pig isolated ileum longitudinal muscle were studied. PGE1 (2.8--28 nM) consistently and dose dependently increased the contractions evoked by CCK (indirect muscle stimulation) or by ACh. IND (2.7 microM) decreased the contractions to both compounds and this was reversed with 2.8--7 nM PGE1. Pretreatment of the preparations with phentolamine (2.6 microM) or pretreatment of the animals with reserpine (2 mg/kg i.p. 24 h before killing) did not affect PGE1 potentiation or IND inhibition of CCK-induced contractions. The results indicated that PGE1 potentiated CCK-induced contractions of the longitudinal muscle of guinea-pig ileum by increasing the response to released ACh. Experiments with IND suggested that endogenous PGs may modulate the effect of CCK or related gastrointestinal hormones.

Acetylcholine↗
PubMed1995

Differential mechanism of peptide YY and neuropeptide Y in inhibiting motility of guinea-pig colon.

The effect of peptide YY on contractility, acetylcholine release and noradrenaline release was examined in the isolated guinea-pig colon, and findings were compared with those for neuropeptide Y. Peptide YY and neuropeptide Y inhibited the twitch contractions mediated by the stimulation of cholinergic neurons. Peptide YY, neuropeptide Y, [Leu31,Pro34]neuropeptide Y and neuropeptide Y-(13-36) inhibited the electrically stimulated release of acetylcholine. Neuropeptide Y, but not peptide YY, inhibited the high K(+)-stimulated tetrodotoxin-resistant release of acetylcholine, while the inhibitory effect of neuropeptide Y disappeared after treatment with yohimbine. Neuropeptide Y, but not peptide YY or neuropeptide Y analogues, evoked the release of noradrenaline. After desensitization to the effects of neuropeptide Y, peptide YY inhibited electrically stimulated acetylcholine release. Thus, peptide YY inhibits acetylcholine release through stimulation of a receptor, distinct from the site of action of neuropeptide Y, located on cholinergic neurons as well as the neuropeptide Y Y1 and Y2 receptors in the guinea-pig colon. Neuropeptide Y inhibits acetylcholine release due to the noradrenaline release mediated by stimulation of a receptor distinct from neuropeptide Y Y1 and Y2 receptors, located on adrenergic neurons.

Acetylcholine↗