Somatostatin and the Stomach

Ertan, Atilla; Arimura, Akira

doi:10.1159/000171158

Dig Dis

1987

DOI: 10.1159/000171158

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Somatostatin and the Stomach

Atilla Ertan¹,

Akira Arimura²

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1988

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Cited by 8 publications

(1 citation statement)

References 38 publications

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“…Somatostatin, the peptide stored by and released from the D cells, is a candidate hormone for inhibition of gastric acid secretion (8)(9)(10)(11). The role of these gastrointestinal peptides and amines in acid peptic disorders is related to possible increased stimulation of parietal cells by gastrin (12)(13)(14)(15), somatostatin deficiency, or dysfunction of G cells, D cells or both (16)(17)(18)(19). The present investigation examines the distribution and ratio of gastrin-secreting G cells, somatostatinsecreting D cells and serotonin-secreting EC cells in the stomach and duodenum of patients with acid peptic disorders.…”

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confidence: 99%

Immunocytochemical and Morphometric Studies of Gastrin‐, Somatostatin‐ and Serotonin‐Producing Cells in the Stomach and Duodenum of Patients with Acid Peptic Disorders

Yacoub

Thomson

Hooper

et al. 1996

Canadian Journal of Gastroenterology and Hepatology

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Gastric and duodenal biopsies from 90 patients with various acid peptic disorders-reflux esophagitis (n = 24), gastric ulcer (n = 13), duodenal ulcer (n = 47) and nonulcer dyspepsia (n = 6)-were examined. Seven patients with minimal dyspeptic symptoms and an endoscopically and histologically normal stomach and duodenum served as controls. Immunoperoxidase staining for gastrin-producing G cells, somatostatin-producing D cells and serotonin-producing EC cells was carried out on fundic, antral and duodenal biopsies, and was quantified using a Zeiss MOP Videoplan using the peroxidase-antiperoxidase technique of Sternberger. In the gastric antrum, a G:D:EC cell ratio of approximately 1.6:1:1-was observed. In the duodenum the corresponding ratio was 1:1:2.4. No significant differences were observed within any of the major diagnostic categories. Patient age, sex, duration of symptoms, smoking habits, alcohol consumption and nonsteroidal anti-inflammatory drug use had no effect on endocrine cell densities. Reduced G cell density in the descending duodenum was observed in the presence of mild duodenitis in four patients. In four patients with evidence of antral intestinal metaplastic changes, a significant increase in duodenal G cell densities was found. These results suggest that a change in the number of G, D or EC cells does not play a primary role in the pathophysiology of acid peptic disorders in the majority of patients.

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confidence: 99%

Immunocytochemical and Morphometric Studies of Gastrin‐, Somatostatin‐ and Serotonin‐Producing Cells in the Stomach and Duodenum of Patients with Acid Peptic Disorders

Yacoub

Thomson

Hooper

et al. 1996

Canadian Journal of Gastroenterology and Hepatology

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Gastric luminal somatostatin secretion of normals and patients with pernicious anemia and with Zollinger-Ellison syndrome

et al. 1988

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We studied the release of gastric luminal somatostatin-like immunoreactivity (SLI) in response to a pentagastrin infusion (0.9 microgram/kg/hr, intravenous) in five normal volunteers, five patients with pernicious anemia, and two patients with Zollinger-Ellison syndrome. In addition, we studied the gastric luminal SLI secretion in response to a gastric luminal acid perfusion in two patients with pernicious anemia. Our results have shown that: (1) pentagastrin caused a parallel increase in luminal hydrogen ions and SLI release in normal volunteers; (2) Zollinger-Ellison patients had elevated basal acid and SLI levels that did not increase further with pentagastrin; (3) pentagastrin did not increase gastric acid or luminal SLI secretion in pernicious anemia patients; and (4) in pernicious anemia patients, a gastric luminal acid perfusion caused a significant increase in gastric luminal SLI over baseline values. In conclusion, gastric luminal hydrochloric acid appears to be a factor which stimulates the secretion of luminal SLI in human beings.

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Gastric, duodenal, and pancreatic somatostatin-like immunoreactivity during hypovolemic shock

et al. 1988

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Because hypovolemic shock is known to cause gastric ulcers in animals and human beings, we investigated the tissue levels of somatostatin-like immunoreactivity (SLI) in the gastric corpus and antrum, duodenum, and pancreas during hypovolemic shock in rats. We studied male Wistar rats (N = 10 each) 15 min, 2 hr, and 12 hr after hypovolemic shock and compared results to a control group (N = 15). Two rats in both 2-hr and 12-hr groups showed gastric ulcers: three corporal and one antral. One animal developed multiple ulcers. In the gastric corpus and antrum and in the duodenum, tissue SLI showed significant decrease 15 min and 2 hr after shock. Gastric SLI remained low, whereas duodenal SLI recovered and rose above control level at 12 hr. Pancreatic SLI showed no significant changes during hypovolemic shock. Gastric tissue SLI levels that were significantly lower after shock than those of normal controls may have contributed to the peptic ulcer disease induced by hypovolemic shock in this experimental model.

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Somatostatin and the Stomach

Cited by 8 publications

References 38 publications

Immunocytochemical and Morphometric Studies of Gastrin‐, Somatostatin‐ and Serotonin‐Producing Cells in the Stomach and Duodenum of Patients with Acid Peptic Disorders

Immunocytochemical and Morphometric Studies of Gastrin‐, Somatostatin‐ and Serotonin‐Producing Cells in the Stomach and Duodenum of Patients with Acid Peptic Disorders

Gastric luminal somatostatin secretion of normals and patients with pernicious anemia and with Zollinger-Ellison syndrome

Gastric, duodenal, and pancreatic somatostatin-like immunoreactivity during hypovolemic shock

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