Somatostatin receptor subtype 2 mediates inhibition of gastrin and histamine secretion from human, dog, and rat antrum

Zaki, Muhammad; Harrington, Leslie; McCuen, Robert W.; Coy, David H.; Arimura, Akira; Schubert, Mitchell L.

doi:10.1016/s0016-5085(96)70059-8

Cited by 53 publications

(21 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The decrease in ghrelin concentrations may reflect a direct inhibitory action of somatostatin on ghrelin-releasing peripheral cells and may indicate a continuous constitutive release of ghrelin under normal conditions. It is well known that somatostatin inhibits hormone release from neuroendocrine cells (33) and that the gastrointestinal mucosa expresses somatostatin receptors (34). Thus, there could also be an interaction between somatostatin and the ghrelin-producing cells, but so far there is no direct evidence to support this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Plasma Ghrelin Concentrations Are Not Regulated by Glucose or Insulin

Schaller¹,

Schmidt

Pleiner³

et al. 2003

Diabetes

185

117

View full text Add to dashboard Cite

Ghrelin plasma concentrations increase during fasting and fall rapidly after nutrient ingestion. We hypothesized that insulin or glucose could regulate ghrelin secretion by a feedback mechanism. In this randomized, double-blind, placebo-controlled crossover study, three different study days were carried out in nine healthy volunteers (age 26 ؎ 6 years). On each day, stepwise increasing systemic glucose concentrations of 5.0, 8.3, and 11.1 mmol/l were attained by intravenous infusion of glucose, representing fasting and postprandial conditions. Ghrelin plasma concentration was studied during concomitant exogenous hyperinsulinemia, inhibition of endogenous insulin production by somatostatin infusion, and placebo time control, respectively. Elevated glucose concentrations increased circulating insulin to 612 ؎ 85 pmol/l (P < 0.01), but they did not affect ghrelin concentrations. Prolonged hyperinsulinemia by exogenous infusion resulted in circulating insulin of 1,602 ؎ 261 pmol/l (P < 0.01) and suppressed plasma ghrelin to 49.6% of baseline (P < 0.01). During administration of somatostatin, insulin concentration remained constant, but an even greater decrease in ghrelin to 39.5% of baseline was noted (P < 0.01). Hyperglycemia does not decrease ghrelin, and a reduction in ghrelin is only seen at supraphysiological insulin concentrations. In contrast, systemic ghrelin concentrations are decreased by somatostatin. The meal-related suppression of ghrelin appears not directly regulated by glucose or insulin.

show abstract

Section: Discussionmentioning

confidence: 99%

Plasma Ghrelin Concentrations Are Not Regulated by Glucose or Insulin

Schaller¹,

Schmidt

Pleiner³

et al. 2003

Diabetes

185

117

View full text Add to dashboard Cite

show abstract

“…Although the five somatostatin receptor subtypes are localized in the stomach (Prinz et al, 1994;Le Romancer et al, 1996;Krempels et al, 1997;Sternini et al, 1997;Schindler & Humphrey, 1999), functional in vivo studies in rats, dogs, and mice as well as in vitro studies in human, rat, and dog antral tissue suggest that somatostatin effects on gastric acid secretion are mediated through the activation of SSTR2 receptors located primarily on ECL cells, where they inhibit the release of histamine (Rossowski et al, 1994;Lloyd et al, 1995;Zaki et al, 1996;Aurang et al, 1997;Fung & Greenberg, 1997;Martinez et al, 1998;Patel, 1999;Martinez, 2002;Piqueras et al, 2003b). In addition, somatostatin also regulates gastrin gene expression and gastrin release from G cells (Karnik et al, 1989;Chiba & Yamada, 1994).…”

Section: Introductionmentioning

confidence: 99%

Peripheral PACAP inhibits gastric acid secretion through somatostatin release in mice

Piqueras

Taché

Martı́nez

2004

British J Pharmacology

View full text Add to dashboard Cite

1 Studies in rats suggest that PACAP modulates gastric acid secretion through the release of both histamine and somatostatin. 2 We characterized the effects of exogenous PACAP on gastric acid secretion in urethaneanesthetized mice implanted with a gastric cannula and in conscious 2-h pylorus ligated mice, and determined the involvement of somatostatin and somatostatin receptor type 2 (SSTR2) by using somatostatin immunoneutralization, the SSTR2 antagonist, PRL-2903, and SSTR2 knockout mice. ). Somatostatin antibody and PRL-2903 increased basal secretion in wild-type mice but not in SSTR2 knockout animals. 4 In wild-type urethane-anesthetized mice, PACAP-38 (3-270 mg kg À1 h À1 ) did not affect the low basal acid secretion, but inhibited the acid response to pentagastrin, histamine, and bethanechol. 5 In wild-type urethane-anesthetized mice pretreated with somatostatin antibody or PRL-2903 and in SSTR2 knockout mice, peripheral infusion of PACAP-38 or somatostatin-14 did not inhibit the increased basal gastric acid secretion. 6 In conscious wild-type mice, but not in SSTR2 knockout mice, PACAP-38 inhibited gastric acid secretion induced by 2-h pylorus ligation. The antisecretory effect of PACAP-38 was prevented by immunoneutralization of somatostatin. 7 These results indicate that, in mice, peripheral PACAP inhibits gastric acid secretion through the release of somatostatin and the activation of SSTR2 receptors. There is no evidence for stimulatory effects of PACAP on acid secretion in mice.

show abstract

“…PHC was measured by a commercial immunoassay 14 This assay has been validated for in vitro or in vivo use in the dog. [15][16][17] PHCs in dogs with MCTs were compared to those in control dogs (3 intact male and 2 intact female adult healthy Beagles).…”

Section: Sample Preparation and Plasma Histamine Assaymentioning

confidence: 99%

Relationship of Disease Progression and Plasma Histamine Concentrations in 11 Dogs with Mast Cell Tumors

Ishiguro¹,

Kadosawa²,

Takagi³

et al. 2003

J Vet Int Med

View full text Add to dashboard Cite

Plasma histamine concentrations (PHCs) were measured serially over 9 months or until death in 11 dogs with mast cell tumors (MCTs). Eight dogs had grossly visible disease and the other 3 dogs had microscopic disease. Initial PHCs in the dogs with gross disease were significantly higher than PHCs in healthy dogs (median, 0.73 ng/mL and 0.19 ng/mL respectively; P Ͻ .009), whereas initial PHCs in dogs with microscopic disease showed no difference from controls. Seven dogs subsequently had progressive increases in PHC, and developed hyperhistaminemia (median, 14.0 ng/mL; range, 5.11-30.1 ng/mL). These 7 dogs died from MCTs, and 1 had general weakness with rapid lysis of a large tumor burden after radiation therapy. PHCs of the other 4 dogs were less than 1 ng/mL during the study. These 4 dogs were still alive with adequate control of the tumor at the conclusion of the study. Four of the 11 dogs initially had gastrointestinal (GI) signs, which abated soon after administration of histamine-2 (H-2) blockers. No significant difference was found between PHCs in dogs with GI signs and those without GI signs (median, 0.86 ng/mL and 0.35 ng/mL, respectively). Thereafter, 7 dogs had serious GI complications for which H-2 blocker therapy was ineffective. PHCs in these 7 dogs were extremely high (median, 12.2 ng/mL; range, 3.42-30.1 ng/mL). Results of this study demonstrated that PHC was one factor related to disease progression, and indicated that marked hyperhistaminemia was associated with the GI signs refractory to H-2 blocker therapy in dogs with MCTs.

show abstract

Somatostatin receptor subtype 2 mediates inhibition of gastrin and histamine secretion from human, dog, and rat antrum

Cited by 53 publications

References 4 publications

Plasma Ghrelin Concentrations Are Not Regulated by Glucose or Insulin

Plasma Ghrelin Concentrations Are Not Regulated by Glucose or Insulin

Peripheral PACAP inhibits gastric acid secretion through somatostatin release in mice

Relationship of Disease Progression and Plasma Histamine Concentrations in 11 Dogs with Mast Cell Tumors

Contact Info

Product

Resources

About