Expression of progastrin derived peptides and somatostatin in fundus and antrum of non-ulcer dyspepsia subjects with and without Helicobacter pylori infection

Zavros, Yana; Paterson, Adrienne C.; Lambert, John; Shulkes, Arthur

doi:10.1016/s0016-5085(00)81179-8

Cited by 6 publications

(8 citation statements)

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“…Recent studies have clearly demonstrated that antral, but not corpus, SST levels were decreased in H. pylori infection, by measuring the SST concentration in specimens biopsied from both sites. 31,32 In the same year, 1992, as our study above, 30 Moss et al 33 demonstrated that eradication of H. pylori from 10 DU patients caused approximately twofold increases in SST messenger RNA (mRNA) in antral, but not in corpus biopsies. They also showed an increase in D cell numbers after H. pylori eradication in 18 subjects with active DU.…”

Section: Conventional Human Study Of Somatostatin In H Pylori Infectionsupporting

confidence: 52%

“…Effects of ammonia solution, administered orally for 2 weeks (white bars) or 4 weeks (black bars), on the number (nb) of somatostatin (D)-, and somatostatin receptor subtype 2 (SSTR-2) peptide[31][32][33][34][35][36][37][38][39][40][41]-labeled cells per unit area (0.29 mm 2 ) in the antral mucosa, and on portal gastrin levels in rats. Each bar represents the mean Ϯ SE value of five rats.…”

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confidence: 99%

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Helicobacter pylori and gut hormones

Kaneko

Konagaya

Kusugami

2002

Journal of Gastroenterology

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Helicobacter pylori infection has been found to decrease the expression of antral somatostatin and to increase the release of the acid-stimulating hormone gastrin. The reversal of these changes in gut hormones by the eradication of H. pylori, and in-vivo and in-vitro studies in animals either infected with H. pylori or exposed to H. pylori-related materials may support the somatostatin-gastrin link theory in the pathophysiology of H. pylori infection. The following mechanisms have been proposed to explain the H. pylori infection-associated changes in gut hormones; (1) ammonia produced by H. pylori and monochloramine, (2) effect on somatostatin receptor subtype-2, (3) action of lipopolysaccharide from H. pylori on somatostatin receptor, (4) inflammatory cells and mediators, and (5) bacterial strain diversity. H. pylori infection can alter gastric acid secretion in both directions. The elevated acid secretion in patients with duodenal ulcer is decreased by H. pylori eradication, and is accompanied by the normalization of gut hormones in patients whose H. pylori-induced gastritis is limited to the antrum with hyperacidity. Corpus gastritis and the subsequent development of mucosal atrophy induced by H. pylori result in decreased acid secretion, although the mechanism underlying H. pylori-induced atrophy in some subjects remains unclear. Hypoacidity enhances corpus atrophy and increases gastrin secretion, mediated via a physiological suppression of somatostatin release, features that are also observed in H. pylori infection. Therefore, the capacity of acid secretion and distribution of gastritis or atrophy should be taken into consideration when we discuss the affect of H. pylori on gut hormones.

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Section: Conventional Human Study Of Somatostatin In H Pylori Infectionsupporting

confidence: 52%

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confidence: 99%

Helicobacter pylori and gut hormones

Kaneko

Konagaya

Kusugami

2002

Journal of Gastroenterology

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“…Mihaljevic et al [3] showed that the level of serum SS in Hp+ patients was lower than that in Hp-patients. Zavros et al [12] found that the content of SS in specimens of gastric mucosa from chronic gastritis Hp+ patients was 6 times lower than that in chronic gastritis Hp-patients. Chavialle et al [13] showed that the content of SS in gastric antrum mucosa of DU patients was lower than that in the control group.…”

Section: Discussionmentioning

confidence: 97%

Assay of gastrin and somatostatin in gastric antrum tissues of children with chronic gastritis and duodenal ulcer

Xie

Zhao²,

Qi³

et al. 2006

WJG

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AIM:To study the expressions of gastrin (GAS) and somatostatin (SS) in gastric antrum tissues of children with chronic gastritis and duodenal ulcer and their role in pathogenic mechanism. METHODS:Specimens of gastric antrum mucosa from 83 children were retrospectively analyzed. Expressions of GAS and SS in gastric antrum tissues were assayed by the immunohistochemical En Vision method. RESULTS:The expressions of GAS in chronic gastritis Hp+ group (group A), chronic gastritis Hp-group (group B), the duodenal ulcer Hp + group (group C), duodenal ulcer Hp-group (group D), and normal control group (group E) were 28. 50 + 4.55, 19.60 + 2.49, 22.69 + 2.71, 25.33 + 4.76, and 18.80 + 2.36, respectively. The value in groups A-D was higher than that in group E. The difference was not statistically significant. The expressions of SS in groups A-E were 15.47 + 1.44, 17.29 + 2.04, 15.30 + 1.38, 13.11 + 0.93 and 12.14 + 1.68, respectively. The value in groups A-D was higher than that in group E. The difference was also not statistically significant. CONCLUSION:The expressions of GAS and SS are increased in children with chronic gastritis and duodenal ulcer.

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“…SST deficiency had been proposed in duodenal ulcer patients before the discovery of H. pylori (3). Recent studies have clearly demonstrated that antral SST levels were decreased in H. pylori infection (20,21). Like SST and gastrin, it was likely that ghrelin could be affected by H. pylori infection.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori has no effect on plasma ghrelin levels

Gökçel

Gümürdülü

Kayaselçuk

et al. 2003

European Journal of Endocrinology

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Objective: Helicobacter pylori is the major etiologic agent for chronic active gastritis, and it also plays a crucial role in gastric and duodenal ulcer disease, as well as in gastric carcinoma. H. pylori infection has been shown to decrease plasma somatostatin (SST) and increase plasma gastrin concentrations. Ghrelin is a recently discovered peptide produced mostly in the stomach of rodents and humans and is secreted into the bloodstream. There is no data in the literature about the relationship between H. pylori and ghrelin. Design: Thirty-nine age-and BMI-matched H. pylori infection positive and negative women, from whom biopsy specimens were taken during gastric endoscopy, were included in the study. Methods: Total ghrelin was measured by enzyme immunoassay (EIA) in Medistek. All samples were measured in duplicate and averaged; results differing by more than 20% were re-assayed. Two biopsy specimens from antrum, corpus and fundus were obtained. Results: Fifteen of the subjects were H. pylori negative and 24 were H. pylori positive. Age, BMI, lipid profile and insulin sensitivity indices of the groups were similar. Plasma ghrelin levels ð375:92^7:10 vs 370:00^4:14 pmol=l; P . 0:05Þ of H. pylori negative and positive groups did not differ significantly. Conclusion: H. pylori has no effect on plasma ghrelin concentration.

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Expression of progastrin derived peptides and somatostatin in fundus and antrum of non-ulcer dyspepsia subjects with and without Helicobacter pylori infection

Cited by 6 publications

References 0 publications

Helicobacter pylori and gut hormones

Helicobacter pylori and gut hormones

Assay of gastrin and somatostatin in gastric antrum tissues of children with chronic gastritis and duodenal ulcer

Helicobacter pylori has no effect on plasma ghrelin levels

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