SEARCH · PubMed Health

Results for “ENTEROGASTRONE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1992

Endogenous secretin in the rat--evidence for a role as an enterogastrone but failure to influence serum calcium homeostasis.

The release of secretin into plasma by intraduodenal (id) infusion of HCl or iso-osmotic (290 mosm l-1) NaCl, and the associated changes of moderately stimulated gastric acid, serum gastrin, two calciotropic hormones, total and 45calcium (Ca), were examined in the rat. The possible role of endogenous secretin as an enterogastrone and as a mediator of the hypothesized endocrine gut-thyroid-parathyroid axis was further characterized with the aid of secretin immunoneutralization and exogenous secretion. The id-HCl-stimulated secretin, measured by a sensitive radioimmunoassay, was accompanied by a decrease in gastric acid secretion, whereas secretin blockage by anti-secretin immune serum resulted in a significant increase in acid secretion. The correlation between plasma secretin and acid output was only slight. Gastrin and Ca metabolism remained unchanged during secretin stimulation. Intravenous synthetic porcine secretin at a dose reported to be effective in other target preparations (2 CU (0.58 microgram) kg-1 h-1) had no effect on gastric acid secretion and Ca metabolism. In contrast, a pharmacological dose, 32 CU (9.3 micrograms) kg-1 h-1, inhibited acid secretion, decreased serum Ca and total protein, and increased serum parathyroid hormone, but left calcitonin and gastrin unchanged. Endogenous secretin appeared to act as an enterogastrone, but whether it was the only one is unclear. No role was detected for secretin in the gut-thyroid-parathyroid axis, since the Ca changes observed may have been unspecifically mediated.

Animals↗

PubMed1986

Enterogastrone-like effect of peptide YY is vagally mediated in the dog.

Intraluminal fat inhibits gastric secretion through as yet undetermined mechanisms which involve release of one or more hormonal enterogastrones. As intraluminal fat releases Peptide YY (PYY) in amounts sufficient to inhibit meal-stimulated acid secretion, this ileo-colonic peptide exhibits the characteristics required of an enterogastrone. The present study seeks to determine the mechanism by which PYY inhibits acid secretion by examining the effects of PYY on gastric acid stimulated by pentagastrin, histamine, and bethanechol. In addition, effects of PYY on the acid response to sham feeding and distention of a denervated gastric pouch were examined. A dose of PYY (400 pmol X kg-1 X h-1) was employed that reproduced blood levels observed after intestinal perfusion with oleic acid and inhibited the acid secretory response to an intragastric meal by 35 +/- 6%. This same dose of PYY maximally inhibited histamine- and pentagastrin-stimulated acid secretion by 28 +/- 7% (P less than 0.05), and 17 +/- 4% (P less than 0.05), respectively. Although PYY had no effect on bethanechol-stimulated secretion it markedly inhibited the secretory response to sham feeding, maximally reducing secretion by 90 +/- 4% (P less than 0.01). We speculate that PYY acts by inhibiting acetylcholine release from vagal nerve fibers rather than by inhibiting acetylcholine's action on the parietal cell. The demonstration that PYY virtually abolishes cephalic phase acid secretion while having little if any effect on the response to exogenous secretogogues gives PYY unique characteristics among the known hormonal inhibitors of gastric secretion.

Animals↗

PubMed1977

The effect of vagotomy on the canine enterogastrone mechanism.

The effect of truncal vagotomy on the enterogastrone mechanism was evaluated in dogs with Heidenhain pouches and gastric and pancreatic fistulas. During continuous infusion of pentagastrin, 8 microg-Kg.-hr., HCl was infused into the duodenum in doses of 12, 18, and 24 mEq. per hour before and one month following transthoracic vagotomy. The effect of vagotomy on the inhibition of pentagastrin-stimulated Heidenhain pouch hydrogen ion output produced by the endogenous release of duodenal hormones was evaluated. The results indicate that there was no difference in the degree of inhibition produced by 12 and 18 mEq. intraduodenal HCl before and after vagotomy. When 24 mEq. per hour HCl was infused, the percent inhibition was significantly greater after vagotomy compared to values before vagotomy. The D50 of intraduodenal acid for inhibition of Heidenhain pouch hydrogen ion output was not altered by vagotomy, whereas the calculated maximal response (inhibition) was increased after vagotomy. Pancreatic volume was greater after vagotomy when compared to values before vagotomy, when 24 mEq. of HCl per hour was infused into the duodenum. These data suggest that vagotomy does not impair the effectiveness of the enterogastrone mechanism and at high doses of intraduodenal acid may augment it.

Animals↗

PubMed2004

Gastric emptying, gastric secretion and enterogastrone response after administration of milk proteins or their peptide hydrolysates in humans.

BACKGROUND: The influence of protein fractionation on gastric emptying and rate of appearance of their constituent amino acids in peripheral blood remains unknown. AIM OF THE STUDY: To examine the influence of the degree of protein fractionation on gastric emptying, gastric secretion, amino acid absorption and enterogastrone response, after the intragastric administration of complete cow milk proteins or their respective peptide hydrolysates in man. METHODS: Six healthy males were randomized to receive one of the following four solutions: whey whole protein (W), casein whole protein (C), whey peptide hydrolysate (WHY) or casein hydrolysate (CAHY). All solutions were matched for volume (600 mL), nitrogen content (9.3 g/L), energy density (1069-1092 kJ/L), osmolality (288-306 mosmol/kg), pH (6.9-7.0) and temperature (37 degrees C). RESULTS: Solutions were emptied at similar rates, with mean half-times of (mean +/- SEM) 21.4 +/- 1.3, 19.3 +/- 2.2, 18.0 +/- 2.5 and 19.4 +/- 2.8 min, for the WHY, CAHY, C and W, respectively. The rates of intestinal absorption of water and amino acids were similar with the exception of the casein protein solution, for which the speed of intestinal amino acid absorption was slower (p < 0.05). The peptide hydrolysates elicited about 50% more gastric secretion than the whole protein solutions ( p < 0.05),which was accompanied by higher glucose-dependent insulinotropic polipeptide (GIP) plasma levels during the first 20 min of the gastric emptying process. Similar glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) plasma responses were elicited by the four solutions. CONCLUSIONS: The rate of gastric emptying and the plasma GLP-1 and PYY responses to feeding with cow milk protein solutions in humans are independent of the degree of protein fractionation and are not altered by small differences in the amino acid composition or protein solubility. In contrast, the GIP response is accentuated when milk proteins are delivered as peptide hydrolysates.

Adult↗

PubMed1970

Further purification of a polypeptide demonstrating enterogastrone activity.

1. The further purification of a polypeptide having potent enterogastrone activity, without CCK-PZ effects, is described.2. The material was inhibitory when doses of 1.0 mug/kg.hr were administered intravenously. Amino acid analyses demonstrated the absence of proline, a high content of glutamine and a preponderance of lysine over arginine. Tryptic degradation destroys the inhibitory effect of the polypeptide. Further studies must be performed before the physiological status of the polypeptide can be ascertained.

Alginates↗

PubMed1981

Secretin is an enterogastrone in the dog.

To determine the physiological significance of secretin on gastric secretion, effects of normal rabbit serum (control) and rabbit antisecretin serum (anti-S) on meat meal-stimulated gastric secretion of acid and pepsin from vagally innervated fundic pouches were studied in four dogs with gastric fistulas. The intravenous administration of control serum did not affect the postprandial rise in plasma secretin concentration, whereas intravenous anti-S virtually eliminated the circulating plasma secretin. Both plasma gastrin concentration and acid output following intravenous anti-S were significantly greater than those following intravenous control serum. However, pepsin outputs in the two groups of experiments were not significantly different. In the same dogs in the fasting state, during intravenous infusion of secretin in doses of 0.06 and 0.125 U . kg-1 . h-1, the acid output stimulated by intravenous human synthetic gastrin in a dose of 0.25 micrograms . kg-1 . h-1 was significantly less than that during intravenous saline. The studies indicate that secretin in a physiological dose can inhibit postprandial release of gastrin and gastric secretion of acid, and thus secretin is an enterogastrone in the dog.

Animals↗

PubMed1997

Candidate canine enterogastrones: acid inhibition before and after vagotomy.

The relative contributions of several gut-derived peptides as enterogastrones known to be released in response to a fatty meal and to inhibit acid secretion have not previously been compared directly. We determined the acid-inhibitory activities of increasing intravenous doses of several peptides before and after highly selective vagotomy (HSV) during intragastric titration of a peptone meal in dogs. Before HSV, threshold inhibitory doses of peptide YY (PYY), cholecystokinin (CCK), and secretin were 5, 7, and 10 pmol.kg-1.h-1, respectively, whereas neurotensin, glucagon-like peptide-1 (GLP-1), and oxyntomodulin failed to inhibit acid secretion at doses up to 1,000 pmol.kg-1.h-1. The calculated dose producing 50% acid inhibition (ID50) of secretin (62 pmol.kg-1.h-1) was one-half that of PYY (128 pmol.kg-1.h-1). Maximal (90%) acid inhibition was produced by 100 pmol.kg-1.h-1 secretin and 500 pmol.kg-1.h-1 PYY. The highest dose of CCK that did not cause vomiting (100 pmol.kg-1.h-1) inhibited peptone-stimulated acid output by only 60%. After HSV, 500 pmol.kg-1.h-1. PYY and 200 pmol.kg-1.h-1 CCK failed to inhibit acid output by more than 50%. Threshold doses for inhibition by PYY and CCK were 200 and 100 pmol.kg-1.h-1, respectively. Secretin remained a potent inhibitor after HSV, with an ID50 of 80 pmol.kg-1.h-1 and a threshold dose of 10 pmol.kg-1.h-1. HSV also failed to affect inhibition caused by somatostatin. This study has shown that PYY and secretin are somewhat more potent and efficacious inhibitors of acid secretion than CCK but that all three peptides are far more active than GLP-1, neurotensin, and oxyntomodulin. PYY and CCK inhibit acid secretion in large part through vagal innervation of the gastric fundus, but the inhibitory effects of secretin are independent of fundic vagal innervation.

Animal Feed↗

PubMed1992

Oxyntomodulin-like immunoreactivity: diurnal profile of a new potential enterogastrone.

The biological specificity of oxyntomodulin toward the gastric mucosa results from its C-terminal octapeptide. A RIA using a specific antibody raised against this region permitted quantification of the whole set of proglucagon-derived peptides that interact with the oxyntomodulin recognition systems, corresponding to the new concept of oxyntomodulin-like-immunoreactivity (OLI). The present report describes the physiological 24-h OLI profile in human plasma (eight men and eight women; mean age, 45 yr; range, 20-77 yr). Blood was withdrawn every hour from 0700-1900 h and every 2 h from 2100-0500 h. A meal-dependent profile was found for circulating OLI, with basal values (60 +/- 7 ng/L) at 0500 h and rises elicited by each food intake. The highest value (136 +/- 21 ng/L) was obtained at 2100 h. Plasma concentrations and diurnal variations of OLI were similar to those of the other intestinal peptides known to exert an endocrine function. The mean circulating OLI values increased with age, whereas no change was noticed according to sex. The inhibitory effect exerted by the peptides of the OLI family on gastric acid secretion, the meal dependence of their plasma concentrations, and the observed synchronism of their diurnal profile with that previously described for somatostatin make them candidates for an enterogastrone action.

Age Factors↗

PubMed1980

Gastric inhibitory polypeptide (GIP) is not the primary mediator of the enterogastrone action of fat in the dog.

We compared the inhibition of food-stimulated gastric acid secretion and changes in serum concentrations of immunoreactive gastric inhibitory polypeptide and gastrin caused by: (a) duodenal perfusion of oleic acid, and (b) intravenous infusion of pure, natural, porcine gastric inhibitory, polypeptide in dogs with gastric fistula and pancreatic fistula. A rate of duodenal perfusion of oleic acid (12 ml/hr) which gave near maximal pancreatic protein response was chosen. This dose of oleic acid caused complete suppression of acid response to a meal of liver extract (300 ml of a 15% solution) while elevating serum immunoreactive gastric inhibitory polypeptide modestly. By contrast, intravenous administration of gastric inhibitory polypeptide that raised serum immunoreactive gastric inhibitory polypeptide several fold caused only 40% inhibition of acid response to the same meal. Other effects of duodenal perfusion of oleic acid were exaggeration of pancreatic protein secretion and significant inhibition of gastrin release in response to the meal. Exogenous administration of gastric inhibitory polypeptide, on the other hand, was without significant effect on these responses. These results suggest that, in the innervated dog stomach, the enterogastrone action of fat is not primarily mediated by gastric inhibitory polypeptide.

Animals↗

PubMed1952