Suppression of somatostatin release by duodenogastric reflux in dogs.

Thomas, W. E. G.; Ardill, Joy; Buchanan, K.D.

doi:10.1136/gut.25.11.1230

Cited by 5 publications

(5 citation statements)

References 21 publications

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“…The authors of this study concluded that DGR inhibits somatostatin release. In an animal study, DGR suppressed serum somatostatin levels, but this suppression was not observed in cases of bile diversion (30). However, we believe that no conclusion can be drawn because the number of cells could not be analyzed before the disease developed.…”

Section: Discussionmentioning

confidence: 87%

Mucosal distribution of somatostatin-secreting gastric Delta cells in children with gastrointestinal reflux diseases

Kim,

Na,

Paik

et al. 2023

Front. Pediatr.

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IntroductionGastric delta cells (D-cells) secrete somatostatin, which is the primary paracrine suppressor of acid secretion. The number and distribution of D-cells were investigated in children exhibiting endoscopic findings of duodenogastric and gastroesophageal reflux. This study aimed to determine whether the number of D-cells in the gastric body differs from that in the gastric antrum in children using endoscopic findings.MethodsWe retrospectively used immunohistochemical assessments to determine the number of D-cells in the gastric body and antrum in 102 children who presented with abdominal symptoms. The number and distribution of D-cells were investigated according to symptoms, endoscopic findings of gastroesophageal reflux and duodenogastric reflux, and Helicobacter pylori infection status.ResultsThe average age of the patients was 13.3 ± 3.3 years, and the male-to-female ratio was 1:1.68. The mean number of D-cells per high-power field in the antrum and body did not significantly differ by symptoms. However, these values were significantly lower in the gastric body than in the antrum for all symptoms (p < 0.05). Children with reflux had a higher mean number of D-cells (9.6 ± 8.8) in the gastric body than did those without reflux (4.3 ± 3.4) (p = 0.007). Furthermore, the number of D-cells in the gastric body was marginally significantly lower in Helicobacter pylori-positive children (4.9 ± 6.5) than in Helicobacter pylori-negative children (8.5 ± 8.2) (p = 0.053).ConclusionThe number of D-cells in the gastric body decreased in Helicobacter pylori-positive children but significantly increased in children with duodenogastric reflux. Therefore, somatostatin peptide secretion by D-cells may be a major pathophysiological pathway in gastrointestinal reflux disease.

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Section: Discussionmentioning

confidence: 87%

Mucosal distribution of somatostatin-secreting gastric Delta cells in children with gastrointestinal reflux diseases

Kim,

Na,

Paik

et al. 2023

Front. Pediatr.

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“…One possible explanation could be that DRG, which damages the gastric mucosa by bile acids and pancreatic phospholipase A2, leads to peptic ulcers 20 21 . In addition, some animal studies demonstrated that DGR suppresses somatostatin concentrations and increases intragastric gastrin and acid secretion 18 22 23 24 25 26 . Therefore, DGR may be considered a factor in the pathogenesis of gastric and duodenal ulcers as suggested by some researchers 18 30 31 .…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, studies demonstrated that DGR may suppress the somatostatin concentration that is produced by the alkaline nature or pancreatic component of the reflux, which subsequently results in hypersecretion of acid and hypergastrinemia 18 22 23 24 . DGR may therefore be considered a common factor in the pathogenesis of gastric and duodenal ulcers 23 24 25 26 .…”

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confidence: 99%

Increased Risk of Peptic Ulcers Following a Cholecystectomy for Gallstones

Tsai

Huang

Lin

et al. 2016

Sci Rep

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This retrospective cohort study examined the relationship between a cholecystectomy and the subsequent risk of peptic ulcers using a population-based database. Data for this study were retrieved from the Taiwan Longitudinal Health Insurance Database 2005. This study included 5209 patients who had undergone a cholecystectomy for gallstones and 15,627 sex- and age-matched comparison patients. We individually tracked each patient for a 5-year period to identify those who subsequently received a diagnosis of peptic ulcers. We found that of the 20,836 sampled patients, 2033 patients (9.76%) received a diagnosis of peptic ulcers during the 5-year follow-up period: 674 from the study group (12.94% of the patients who underwent a cholecystectomy) and 1359 from the comparison group (8.70% of the comparison patients). The stratified Cox proportional hazard regressions showed that the adjusted hazard ratio (HR) for peptic ulcers during the 5-year follow-up period was 1.48 (95% CI = 1.34~1.64) for patients who underwent a cholecystectomy than comparison patients. Furthermore, the adjusted HRs of gastric ulcers and duodenal ulcers during the 5-year follow-up period were 1.70 and 1.71, respectively, for patients who underwent a cholecystectomy compared to comparison patients. This study demonstrated a relationship between a cholecystectomy and a subsequent diagnosis of peptic ulcers.

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“…It was also reported that bile reflux could cause hypergastrinemia (26,30,33,34) and inhibit the release of somatostatin (35). Decreased serum levels of somatostatin increased the severity of the symptoms of hypergastrinemia, and in return, hypergastrinemia could increase bile reflux (36).…”

Section: Glandular Stomachmentioning

confidence: 99%