Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ENTEROGASTRONE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 91 records · Page 5Linked to original sources
PubMed1983

[The role of secretin in the control of gastric secretion and emptying in the dog].

It is well established that duodenal acidification strongly inhibits gastric acid secretion, gastric emptying rate and gastrin release. These effects are at least partly mediated via hormonal pathways, but it is not known whether they are mediated by the release of one peptide named in the past enterogastrone, or by several peptides acting together. The effects of duodenal acidification on gastric acid secretion and gastrin release can be reproduced by infusion of small doses of secretin and plasma secretin levels increase during duodenal acidification or after a meal. This peptide is thus the most probable candidate as an enterogastrone. It has however never been clearly shown that administration of low doses of secretin do decrease gastric emptying rate as well as acid secretion. Experiments were performed on four dogs with gastric fistulas. A peptone solution was infused into the stomach. The experiments were repeated during infusion of synthetic secretin. Our results indicate that infusion of low doses of secretin reproduce all the effects of duodenal acidification: a significant inhibition of gastric acid secretion, gastrin release and gastric emptying rate.

Animals↗
PubMed1976

Comparison of vasoactive intestinal peptide (VIP) and secretin in gastric secretion and mucosal blood flow.

VIP and secretin were compared in regard to their effects on gastric acid and pepsin secretion induced by pentagastrin histamine or a peptone meal as well as on gastric mucosal blood flow and meal induced serum gastrin level in conscious dogs provided with gastric fistulas and denervated fundic pouches. Both VIP and secretin caused a dose-related stimulation of basal pepsin outputs and inhibition of pentagastrin-induced acid secretion. VIP, like secretin, inhibited pentagastrin and meal-induced gastric acid secretion but in contrast to secretin it caused inhibition of acid response to histamine. Inhibition of acid secretion by VIP or secretin was accompanied by secondary reduction in gastric mucosal blood flow in tests with pentagastrin or histamine and by depression of the serum gastrin level in tests with a peptone meal. This study indicates that in comparison with secretin, VIP has a wider spectrum of inhibition of stimulated gastric secretion and may be considered as one of the enterogastrones released in the small intestine.

Aminopyrine↗
PubMed1976

Absorption of different elemental diets in a short-bowel syndrome lasting 15 years.

In a patient with total colectomy and only 120 cm of the proximal small bowel remaining after resection for Crohn's disease, comparative studies were performed on the absorption of isocaloric amounts of Vivonex HN, Flexical, Codelid, Jejunal, and Precision LR. These elemental and/or complete diets were fed by a nasogastric tube at a constant rate of 260 ml/hr, 1 cal/ml, 2185-2660 ml per feeding period of 8.4-10.2 hr daily. Discharge of intestinal fluids from the jejunal stoma ranged between 2940 ml (Vivonex HN) to 4760 ml (Jejunal) per daily feeding period, resulting in a net intestinal loss of fluids and dehydration with the exception of Flexical. Jejunostomy discharge on Flexical was only 1325 ml per comparable period. The patient tolerated dietary fat relatively well absorbing 61% of 87 g of fat from Flexical and 60% of 108 g from a natural blenderized diet. The other diets used were either fat-free or with a minimum amount of fat. The second best tolerated diet was Vivonex HN, the feeding of which resulted in the highest intestinal retention of nitrogen (84% of the 16.3 g fed as opposed to 78% of 9.1 g fed in Flexical). Vivonex HN also had the highest intestinal retention of phosphorus. Intestinal fluid absorption was not related to the intestinal transit time measured by a nonabsorbable marker or to the osmolality of diets. Diets containing fat may inhibit secretion by the "enterogastrone-like" effect induced by dietary fat in the remaining bowel. High amino acid content of some of the low-fat diets may release gastrointestinal hormones which stimulate secretion, and the simple carbohydrates prevent fluid absorption. In the short-bowel syndrome with normal functions of the pancreaticobiliary system, diets based on fat and protein hydrolysate should be the nutritional therapy of choice.

Colectomy↗
PubMed1975

Current concepts on physiological control of gastric acid secretion. Clinical applications.

Gastric acid secretion by the parietal cell is a single digestive process involving a continuous interplay between nervous and hormonal stimuli. Gastric acid hypersecretion and hypergastrinemia may represent pathologic disturbance of the normal "gastric phase" of acid secretion (excluded antrum syndrome) or abnormal gastrin secretion from a nongastric source as in the Zollinger-Ellison syndrome. Diagnosis of these two syndromes preoperatively is dependent on immunoassay for serum gastrin. A fall in serum gastrin level after the injection of secretin will distinguish the excluded antrum syndrome from the Zollinger-Ellison syndrome. Which hormone or hormones cause the acid hyposecretion of the watery diarrhea hypokalemia achlorhydria syndrome is still uncertain. Potential candidates include secretin, glucagon (alone or combined with gastrin), vasoactive intestinal peptide and gastric inhibitory polypeptide. Secretin has undergone trials as therapy in peptic ulcer whereas glucagon is under investigation for the treatment of acute pancreatitis because of its dual actions as (1) an enterogastrone and (2) an inhibitor of pancreatic secretion.

Animals↗
PubMed1980

Effect of an intravenous fat preparation on canine gastric secretion.

The effect of intravenous administration of a fat emulsion on canine gastric secretion stimulated by intravenous infusion of amino acids, pentagastrin or insulin was studied. The fat preparation was given at a rate of 30 ml/hour for 2 hours, and its effects were compared with those of a comparable amount of saline solution, each given on three separate occasions in each dog. Fat did not alter the Heidenhain pouch secretion stimulated by intravenous amino acids (1.10 versus 1.11 mmol of hydrogen ion, p greater than 0.9) or the gastrostomy secretion stimulated by intravenous insulin (9.22 versus 9.54 mmol of hydrogen ion, p greater than 0.7) but had a modest inhibitory effect on Heidenhain pouch secretion stimulated by pentagastrin (2.75 versus 3.54 mmol of hydrogen ion, p less than 0.05). These data provide indirect support for the contention that the inhibition of gastric secretion by fat in the gut is mediated by the release of an enterogastrone rather than by a direct effect of absorbed fat. Because gastric stimulation by intravenous fat was not observed in the dog, it seems likely that intravenous fat emulsion can be given to seriously ill patients without fear of an increased likelihood of peptic ulceration due to induced gastric hypersecretion.

Amino Acids↗
PubMed1981

Basal hyposecretion of gastric inhibitory polypeptide after Roux-Y hepaticojejunostomy in man.

We previously showed that basal and pentagastrin-stimulated gastric acid secretion, gastrin in serum and gastrin in antral mucosa were significantly greater in patients with Roux-Y hepaticojejunostomy than in those with choledochoduodenostomy. These findings prompted investigation of basal secretion of gastric inhibitory polypeptide (a peptide with an enterogastrone as well as an insulinogenic effect), insulin and glucose in the same patients. Basal gastric inhibitory polypeptide was significantly lower in patients with Roux-Y hepaticojejunostomy than in those with choledochoduodensotomy, whereas glucose and insulin did not differ in the two groups. No correlation could be demonstrated between gastric inhibitory polypeptide, gastric acid secretion and gastrin, suggesting that hyposecretion of gastric inhibitory polypeptide is not a pathogenetic factor for the hypersecretion of gastric acid secretion in patients with Roux-Y hepaticojejunostomy. Hyposecretion of gastric inhibitory polypeptide and gastric acid hypersecretion in patients with bile diversion seem to be two independent phenomena.

Adult↗
PubMed1983

Gastric acid secretion and gastrointestinal hormone release after biliary reconstruction procedures.

The changes in gastric acid secretion and gastrointestinal hormone release were studied after biliary tract reconstruction to investigate the mechanism of gastric acid hypersecretion after a biliary diversion procedure. At follow-up, gastric acid output in patients with Roux-Y choledochojejunostomy was significantly higher than before the operation. In contrast, in patients with jejunal interposition choledochoduodenostomy, which does not bring about biliary diversion, acid output increased slightly after the operation. Moreover, at follow-up, acid output in the Roux- Y group was slightly higher than it was in the interposition group. Although the fasting levels of plasma gastric inhibitory polypeptide were almost the same in both groups, the loading of a test meal elicited a lower response of plasma gastric inhibitory polypeptide in patients with the Roux- Y procedure than in those with the interposition procedure. Therefore, it is assumed that gastric inhibitory polypeptide, as an enterogastrone after a biliary reconstruction procedure, might have some influence on gastric acid secretion.

Adolescent↗
PubMed1985

Effect of peptide YY on gastric, pancreatic, and biliary function in humans.

The effect of peptide YY (PYY) on gastric and pancreatico-biliary secretion was studied in humans. Peptide YY was infused into groups of 6 healthy volunteers at doses of 0.59, 0.20, and 0.064 pmol X kg-1 X min-1. The two higher doses caused a significant suppression of gastric acid and pepsin output during background stimulation with pentagastrin. The middle dose of PYY (0.20 pmol X kg-1 X min-1) that increased plasma PYY levels by 27 +/- 2 pM caused a 90% +/- 18% (mean +/- SEM; p less than 0.001) reduction in the incremental gastric volume response to pentagastrin. Similarly this dose of PYY caused a substantial inhibition of the acid (77% +/- 14%; p less than 0.005) and pepsin (96% +/- 22%; p less than 0.01) response to pentagastrin; in 2 subjects, pepsin output fell to below basal levels. In contrast, the highest dose of PYY (0.62 pmol X kg-1 X min-1) had no significant influence on duodenal juice volume, output of bicarbonate, trypsin, or bilirubin during low dose stimulation with secretin (0.25 pmol X kg-1 X min-1) and cholecystokinin-8 (0.15 pmol X kg-1 X min-1). Thus PYY concentrations in the circulation similar to those seen after the ingestion of food cause a marked reduction in gastric secretion. This peptide should therefore be considered as one of the possible candidates for the classical enterogastrone.

Adolescent↗
PubMed1986

Peptide YY release by fatty acids is sufficient to inhibit gastric emptying in dogs.

Peptide YY is a candidate enterogastrone localized to endocrine cells of the ileocolonic mucosa. The purpose of the present study was to determine if blood levels of peptide YY observed after perfusion of the intestine with fatty acids are capable of slowing gastric emptying. Gastric emptying of a 300-ml saline meal was monitored during intravenous infusion of normal saline or graded doses of peptide YY. Gastric emptying was significantly inhibited by infusion of peptide YY in doses of 200 and 400 pmol/kg X h. During the saline control study, 229 +/- 12 ml of the 300-ml saline meal emptied by 10 min. This figure was reduced (p less than 0.01) to 110 +/- 28 ml by the infusion of peptide YY at a dose of 200 pmol/kg X h. This dose of peptide YY produced plasma concentrations (delta PYY = 239 +/- 50 pM) that were lower than those seen in response to intestinal perfusion of oleic acid (delta PYY = 395 +/- 55 pM) in the same animals. We conclude that perfusion of the intestine with oleic acid releases peptide YY in amounts sufficient to slow gastric emptying.

Animals↗
PubMed1994

Intracisternal injection of apolipoprotein A-IV inhibits gastric secretion in pylorus-ligated conscious rats.

BACKGROUND/AIMS: Fat feeding increases not only serum but also cerebrospinal fluid concentration of apolipoprotein (apo) A-IV, a protein produced mainly by the small intestine in the rat. We hypothesized that apo A-IV may have a central effect on gastric secretion. METHODS: Gastric juice was collected by the pylorus ligation method. Rats underwent pylorus ligation and received intracisternal injection of apo A-IV under brief isoflurane anesthesia. Two hours after the injection, gastric juice was collected and gastric acid output determined. RESULTS: Intracisternal injection of 0.5 microgram apo A-IV had no effect on gastric secretion. However, gastric acid secretion was significantly inhibited by intracisternal injection of 1 microgram apo A-IV. Furthermore, intracisternal administration of higher doses of apo A-IV (2.0 and 4.0 microgram) resulted in greater inhibition of gastric acid secretion in a dose-dependent manner. On the contrary, 4 micrograms of apo A-I intracisternally injected failed to inhibit gastric acid secretion. Intraperitoneal administration of 15 micrograms of apo A-IV did not alter gastric secretion. CONCLUSIONS: These results suggest that apo A-IV may act in the brain to inhibit gastric acid secretion. Apo A-IV might be a central enterogastrone, which is a gastric inhibitor produced by the small intestine in response to fat feeding.

Animals↗
PubMed1983

Natural purified porcine gastric inhibitory polypeptide (GIP) stimulates exocrine pancreas secretion due to contamination with a cholecystokinin-like substance.

The effects of purified natural gastric inhibitory polypeptide-enterogastrone III (GIP-EG III) and a fraction which is further purified by high pressure liquid chromatography (GIP-HPLC) were investigated on the endocrine and exocrine isolated perfused pancreas of rats. At the dose of 5 ng/ml used for both GIP preparations, only GIP-EG III significantly stimulated volume and amylase secretion of the exocrine pancreas. The response of insulin release to stimulation by GIP-EG III or GIP-HPLC was not significantly different. In the presence of cholecystokinin-octapeptide (CCK-8) at a concentration which gave half-maximal stimulation of amylase secretion, GIP-EG III almost doubled the response of the exocrine pancreas, whereas GIP-HPLC had no additional effect. CCK-8 alone significantly increased total insulin output under hyperglycemic conditions. We conclude that porcine GIP purified by gel chromatography contains a CCK-like substance which can be removed by further purification on high pressure liquid chromatography without affecting the insulinotropic activity. Some of the reported effects of GIP could be due to contamination.

Amylases↗
PubMed1985

The effect of neurotensin and secretin on gastric acid secretion and mucosal blood flow in man.

Neurotensin stimulates pancreatic secretion directly and by potentiating the effect of secretin. Neurotensin also inhibits gastric secretion. Secretin inhibits gastric secretion as well, but whether it also interacts with neurotensin is not known. Secretin is known to inhibit gastric mucosal blood flow (GMBF). The effect of neurotensin on GMBF is not known. Acid secretion (triple lumen perfused orogastric tube) and GMBF ([14C]aminopyrine clearance) were therefore measured in 6 subjects during neurotensin, secretin and neurotensin plus secretin infusions. Neurotensin plus secretin reduced acid secretion by a median 130 (range 34-394) mumol/min which was significantly greater than either neurotensin at 36 (7-67) mumol/min or secretin 54 (20-347) mumol/min alone (P less than 0.05). This effect appeared independent of GMBF. Neurotensin plus secretin reduced GMBF by 14 (12-27) ml/min but not significantly more than neurotensin at 11 (3-20) ml/min or secretin 18 (2-27) ml/min alone. Further, there was no correlation between changes in acid output and GMBF during infusion of the peptides. We conclude that the inhibitory effects of neurotensin and secretin on gastric secretion are at least additive and together they may function as an 'enterogastrone'.

Adult↗
PubMed1986

Functional receptors for VIP, GIP, glucagon-29 and -37 in the HGT-1 human gastric cancer cell line.

Three separate sets of receptors sensitive to VIP, GIP and pancreatic/entero-glucagons, have been characterized in HGT-1 cells. The order of relative potencies of VIP receptor agonists was VIP greater than rh GRF-43, rh GRF-29 greater than PHI greater than hp GRF-40, secretin. G-37 was about 4 times less potent than G-29 in HGT-1 cells (G-29 greater than G-37), whereas it was about 20 times more potent than G-29 in rat fundic glands (G-37 greater than G-29). Adenylate cyclase in HGT-1 cells was stimulated by VIP, G-29, G-37 and GIP, over a concentration from 3.16 X 10(-9) to 3.16 X 10(-7) M GIP. The experimental data: (1) support the enterogastrone activity of GIP, via adenylate cyclase activation and somatostatin release by gastric D cells; (2) demonstrate that HGT-1 cells originating from a human fundic tumor are sensitive to the glucagon-like peptides G-29 and -37, as rat fundic glands; (3) indicate that the pharmacological properties of the VIP receptor in this human gastric cell line are similar to those characterized in normal human gastric glands.

Adenylyl Cyclases↗
PubMed1994

Somatostatin is released in response to cholecystokinin by activation of type A CCK receptors.

Cholecystokinin is a principal mediator of intestinal fat-induced inhibition of gastric acid secretion, indicating that it is an important physiological enterogastrone. Cholecystokinin has been shown to inhibit acid secretion by activation of type A CCK receptors and through a mechanism involving somatostatin. In the present study, we investigated the possibility that these two mechanisms are directly related such that activation of type A CCK receptors by CCK causes the release of somatostatin. We tested this hypothesis in vivo in a study of CCK-stimulated release of somatostatin in dogs and in vitro in a study of CCK-stimulated release of somatostatin from an enriched culture of canine fundic D cells. In dogs, IV infusion of CCK (50 pmol/kg/h, IV) significantly increased circulating somatostatin concentrations above basal. Further, systemic administration of somatostatin MAb F(ab)1 fragments of a somatostatin monoclonal antibody prevented most of CCK-induced inhibition of meal-stimulated acid secretion. In canine fundic D cells in culture, CCK-stimulated somatostatin release was blocked in a dose-dependent fashion by application of a type A CCK receptor antagonist. This study indicates that CCK activates type A CCK receptors to release somatostatin from canine fundic mucosal D cells, and accounts for somatostatin-dependent CCK-induced inhibition of acid secretion.

Acids↗
PubMed1994

Activity of oxyntomodulin on gastric acid secretion induced by histamine or a meal in the rat.

Conscious rats with chronic gastric fistula were trained for drinking a 14-ml milk meal. The activity of an intestinal hormone, oxyntomodulin (OXM), was studied in this model and compared to that observed when histamine was the stimulus. Under histamine (0.25 mg.kg-1.h-1) stimulation, OXM at doses (60-120 pmol.kg-1.h-1) that induced physiological circulating levels inhibited gastric acid secretion up to 50%. Under meal stimulation, OXM reduced up to 29% acid secretion at doses (1-1.5 nmol.kg-1.h-1) inducing supraphysiological levels. We conclude that at physiological concentrations OXM cannot counteract the complex processes triggered by a meal. OXM would be a component of enterogastrone, a combination of several intestinal hormones acting in synergy. The OXM action is related to pathways recognizing the C-terminal 19-37 moiety of the molecule.

Animals↗
PubMed2005

The physiological role of GLP-1 in human: incretin, ileal brake or more?

The proglucagon-derived peptide glucagon-like peptide-1 (GLP-1) is an intestinal signal peptide postprandially released from the L cells of the lower gut. Exogenously administered the synthetic hormone exerts a glucose-dependent insulinotropic effect at the pancreatic beta-cells and lowers plasma glucagon by an inhibitory effect against the alpha-cells. It delays gastric emptying by relaxation of the gastric fundus, inhibition of antral contractility, and stimulation of both the tonic and phasic motility of the pyloric sphincter. Enhancement of insulin, suppression of glucagon, and inhibition of gastric emptying are the main determinants controlling glucose homeostasis with GLP-1. Human studies employing the specific GLP-1 receptor antagonist exendin(9-39) show that endogenously released GLP-1 likewise controls fasting plasma glucagon, stimulates insulin, and influences all the motoric mechanisms known to control gastric emptying. Therefore, GLP-1 is discussed as an incretin hormone and as an enterogastrone in man. Synthetic GLP-1 also suppresses gastric acid and pancreatic enzyme secretion. The inhibitory effects on upper gastrointestinal functions are at least partly mediated by vagal-cholinergic inhibition and may involve interactions with vagal afferent pathways and/or circumventricular regions within the CNS. GLP-1 is a candidate humoral mediator of the 'ileal brake' exerting inhibition of upper gastrointestinal function preventing malabsorption and postprandial metabolic disturbances. As human studies indicate a central action of GLP-1 in reduction of food intake, it is uncertain if this is a consequence of induction of satiety or of transduction of visceral aversive stress signals.

Gastrointestinal Hormones↗
PubMed1998

Amidated and non-amidated glucagon-like peptide-1 (GLP-1): non-pancreatic effects (cephalic phase acid secretion) and stability in plasma in humans.

The incretin and enterogastrone hormone, GLP-1, occurs in an amidated (GLP-1 (7-36) amide; 75%) and a glycine-extended (GLP-1 (7-37); 25%) form. Their effects on the endocrine pancreas are similar and their overall (mainly renal) elimination rates appear to equal. Assuming that they might differentially affect non-pancreatic targets we investigated the effect of GLP-1 (7-37) infused at 0.7 pmol/kg/min on sham-feeding induced acid secretion in six healthy volunteers. The infusion increased the plasma concentrations from 16+/-2 pmol/l to 45+/-2 pmol/l. This was associated with a 61+/-14% decrease in acid output compared to saline and was not significantly different from that previously observed with GLP-1 (7-36) amide infused at the same rate. We then compared the degradation of the two forms in human plasma at 37 degrees C in vitro. T1/2 values were 32+/-3 (7-37) and 42+/-2 min (7-36) amide (P=0.007). The difference in metabolism persisted after addition of diprotin A, an inhibitor of dipeptidyl peptidase IV, the enzyme responsible for the initial degradation of GLP-1 in plasma, and broader enzyme inhibitors. Thus, the only effect of the amidation of GLP-1 seems to be to enhance its survival in plasma.

Adult↗
PubMed1998

Effects of GLP-1 on gastric emptying, antropyloric motility, and transpyloric flow in response to a nonnutrient liquid.

Glucagon-like polypeptide 1 (GLP-1) may be a major enterogastrone, slowing gastric emptying when released by intestinal nutrients. In six conscious dogs, we studied the effects of GLP-1, on antropyloric motility, gastric emptying, and transpyloric flow after instillation of 500 ml of saline into the stomach. The meal was given and recordings were started 15 min after intravenous bolus and infusion of either saline or three different doses of GLP-1. Intravenous GLP-1 produced a dose-related retardation of gastric emptying associated with a decrease in the number and volume of flow pulses in comparison to saline. This change in transpyloric flow was associated with an inhibition of antropyloric pressure waves, a stimulation of isolated pyloric pressure waves, and an increase in basal pyloric tone induced by intravenous GLP-1 infusion. Our findings show that GLP-1 has a potent dose-dependent inhibitory effect on transpyloric flow and gastric emptying. This effect is temporally associated with inhibition of antral "pumping" and stimulation of pyloric "braking" mechanisms.

Animals↗