Candidate canine enterogastrones: acid inhibition before and after vagotomy

1997 ◽  
Vol 272 (5) ◽  
pp. G1236-G1242 ◽  
Author(s):  
K. C. Lloyd ◽  
S. Amirmoazzami ◽  
F. Friedik ◽  
A. Heynio ◽  
T. E. Solomon ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Peptide Yy ◽  
Acid Output ◽  
Gastric Fundus ◽  
Acid Inhibition ◽  
Selective Vagotomy ◽  
Before And After ◽  
Calculated Dose ◽  
Vagal Innervation ◽  
Glucagon Like Peptide 1

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.

Inhibitory effect of PYY on vagally stimulated acid secretion is mediated predominantly by Y1 receptors

1996 ◽  
Vol 270 (1) ◽  
pp. G123-G127 ◽  
Author(s):  
K. C. Lloyd ◽  
D. Grandt ◽  
K. Aurang ◽  
V. E. Eysselein ◽  
M. Schimiczek ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Peptide Yy ◽  
Acid Output ◽  
Inhibitory Effect ◽  
Acid Inhibition ◽  
Molecular Forms ◽  
Gastric Fistula ◽  
Selective Agonist ◽  
Rabbit Intestine ◽  
Y1 Receptors

Two molecular forms of peptide YY (PYY), PYY-(1--36) and PYY-(3--36), are abundant in rabbit intestine and blood. We have previously shown that PYY-(1--36) (PYYI) activates equipotently Y1 and Y2 receptors and PYY-(3--36) (PYY II) is a highly selective agonist for Y2 receptors. In the present study, we examined the effect of exogenous infusion of PYY on vagally stimulated gastric acid secretion in awake rabbits with chronic gastric fistula. To determine the specific PYY receptor(s) that mediates this effect, we used a highly selective Y1 agonist, Pro34-PYY, a synthetic PYY, and a Y2-selective agonist, PYY II. Vagal stimulation of acid secretion was elicited by an intravenous bolus injection of insulin (0.125 U/kg) 30 min after beginning a 180-min intravenous infusion of either PYY I, PYY II, or [Pro34]-PYY after a 50 micrograms/kg i.v. bolus of atropine followed immediately by a 500 micrograms/kg sc injection. During infusion of 200 pmol.kg 1.h-1 PYY I, acid output was significantly inhibited to 45 +/- 13% of maximum acid output 60 min after injection of insulin. Similarly, acid output during infusion of 200 pmol.kg-1.h-1 [Pro34]-PYY was significantly inhibited to 52 +/- 12% of maximum. In contrast, acid output during infusion of 200 pmol.kg-1.h-1 of PYY II was not significantly inhibited (101 +/- 18% of maximum). Infusion of double the dose (400 pmol.kg-1.h-1) of PYY II resulted in acid inhibition (51 = 15% of maximum), whereas infusion of the same dose did not significantly enhance acid inhibition by infusion of either PYY I or [Pro34]-PYY (28 +/- 11 and 42 +/- 15% of maximum). These results indicate that PYY, acting predominantly at Y1 receptors, is a potent inhibitor of vagally stimulated acid secretion in adult rabbits.

Mechanism of oleic acid-induced inhibition on gastric acid secretion in rats

1991 ◽  
Vol 260 (4) ◽  
pp. G564-G570 ◽  
Author(s):  
J. C. Rhee ◽  
T. M. Chang ◽  
K. Y. Lee ◽  
Y. H. Jo ◽  
W. Y. Chey
Keyword(s):  
Oleic Acid ◽  
Acid Secretion ◽  
Peptide Yy ◽  
Acid Output ◽  
Inhibitory Effect ◽  
Rabbit Serum ◽  
Similar Degree ◽  
Normal Rabbit Serum ◽  
Anesthetized Rats ◽  
Acid Acid

We investigated the existence of an enterogastrone in rats induced by duodenal administration of oleic acid. Acid secretion by the luminally perfused stomach was stimulated in anesthetized rats by intravenous infusion of 0.3 micrograms.kg-1.h-1 pentagastrin. Intraduodenal administration of 3 mmol of oleic acid produced a profound inhibition (94%) of pentagastrin-stimulated acid output in 10 rats (P less than 0.01). Of several peptides in plasma including secretin, neurotensin, somatostatin, and peptide YY, only secretin was found to increase significantly (P less than 0.001). A similar degree of inhibition of acid output (93%) was caused by porcine secretin, 5.6 pmol.kg-1.h-1, given intravenously to mimic the plasma level of secretin produced by oleic acid infusion. The inhibitory effect of oleic acid on the acid secretion was completely reversed by intravenous injection of a rabbit antisecretin serum but not by a normal rabbit serum. These observations strongly suggest that the inhibition was mediated via circulating secretin. The inhibition produced by either oleic acid or secretin was completely blocked by indomethacin. The blocking action was completely reversed by intravenous administration of 48 micrograms.kg-1.h-1 prostaglandin E2. We conclude that endogenous secretin is a major enterogastrone released by oleic acid in anesthetized rats and that the inhibitory action of secretin requires endogenous prostaglandins.

scholarly journals Acid inhibition by intestinal nutrients mediated by CCK-A receptors but not plasma CCK

2001 ◽  
Vol 281 (4) ◽  
pp. G924-G930 ◽  
Author(s):  
K. C. Kent Lloyd ◽  
Jiafang Wang ◽  
Travis E. Solomon
Keyword(s):  
Acid Secretion ◽  
Gastric Acid ◽  
Trypsin Inhibitor ◽  
Acid Output ◽  
Liquid Diet ◽  
Acid Inhibition ◽  
Soybean Trypsin Inhibitor ◽  
The Individual

We examined the role of CCK-A receptors in acid inhibition by intestinal nutrients. Gastric acid and plasma CCK and gastrin levels were measured in rats with gastric and duodenal fistulas during intragastric 8% peptone and duodenal perfusion with saline, complete liquid diet (CLD; 20% carbohydrate, 6% fat, and 5% protein), and the individual components of CLD. Acid output was significantly inhibited (50–60%) by CLD, lipid, and dextrose. Plasma CCK was significantly increased by CLD (from 2.6 ± 0.3 to 4.8 ± 0.5 pM) and lipid (4.6 ± 0.5 pM). CCK levels 50-fold higher (218 ± 33 pM) were required to achieve similar acid inhibition by exogenous CCK-8 (10 nmol · kg−1 · h−1 iv). Intestinal soybean trypsin inhibitor elevated CCK (10.9 ± 2.5 pM) without inhibiting acid secretion. The CCK-A antagonist MK-329 (1 mg/kg iv) reversed acid inhibition caused by CLD, lipid, and dextrose. Peptone-stimulated gastrin (21.7 ± 1.9 pM) was significantly inhibited by CLD (14.5 ± 3.6 pM), lipid (12.3 ± 2.2 pM), and dextrose (11.9 ± 1.5 pM). Lipid and carbohydrate inhibit acid secretion by activating CCK-A receptors but not by altering plasma CCK concentrations.

Peptide YY and Glucagon-like Peptide-1 in Morbidly Obese Patients Before and After Surgically Induced Weight Loss

2007 ◽  
Vol 17 (12) ◽  
pp. 1571-1577 ◽  
Author(s):  
Thomas Reinehr ◽  
Christian L. Roth ◽  
Gerit-Holger Schernthaner ◽  
Hans-Peter Kopp ◽  
Stefan Kriwanek ◽  
...  
Keyword(s):  
Weight Loss ◽  
Peptide Yy ◽  
Morbidly Obese ◽  
Obese Patients ◽  
Before And After ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Surgically Induced

scholarly journals Hunger and Satiety Peptides: Is There a Pattern to Classify Patients with Prader-Willi Syndrome?

2021 ◽  
Vol 10 (21) ◽  
pp. 5170
Author(s):  
Marta Bueno ◽  
Ester Boixadera-Planas ◽  
Laura Blanco-Hinojo ◽  
Susanna Esteba-Castillo ◽  
Olga Giménez-Palop ◽  
...  
Keyword(s):  
Cluster Analysis ◽  
Peptide Yy ◽  
Prader Willi Syndrome ◽  
Healthy Controls ◽  
Good Tool ◽  
Before And After ◽  
Hormone Responses ◽  
Glucagon Like Peptide 1 ◽  
Underlying Mechanisms ◽  
Cluster 2

Hyperphagia is one of the main problems of patients with Prader-Willi syndrome (PWS) to cope with everyday life. The underlying mechanisms are not yet well understood. Gut-brain hormones are an interrelated network that may be at least partially involved. We aimed to study the hormonal profile of PWS patients in comparison with obese and healthy controls. Thirty adult PWS patients (15 men; age 27.5 ± 8.02 years; BMI 32.4 ± 8.14 kg/m2), 30 obese and 30 healthy controls were studied before and after eating a hypercaloric liquid diet. Plasma brain-derived neurotrophic factor (BDNF), leptin, total and active ghrelin, peptide YY (PYY), pancreatic polypeptide (PP), Glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and amylin were determined at times 0′, 30′, 60′ and 120′. Cluster analysis was used. When considering all peptides together, two clusters were established according to fasting hormonal standardized concentrations. Cluster 1 encompassed most of obese (25/30) and healthy controls (28/30). By contrast, the majority of patients with PWS were located in Cluster 2 (23/27) and presented a similar fasting profile with hyperghrelinemia, high levels of leptin, PYY, GIP and GLP-1, compared to Cluster 1; that may reflect a dysfunction of these hunger/satiety hormones. When peptide behavior over the time was considered, PP concentrations were not sustained postprandially from 60 min onwards in Cluster 2. BDNF and amylin did not help to differentiate the two clusters. Thus, cluster analysis could be a good tool to distinguish and characterize the differences in hormone responses between PWS and obese or healthy controls.

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