Functional anatomy and physiology of gastric secretion

Schubert, Mitchell L.

doi:10.1097/mog.0000000000000213

Cited by 44 publications

(38 citation statements)

References 38 publications

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“…Gastrin also has been shown to induce other EGFR ligands such as heparin-binding EGF,53, 54, 55 as well as trefoil family factor 2 expression 56, 57. The end result of CCK-BR signaling involves motility, 58 secretion, 59 and migration, 60 as well as growth and proliferation 26 . In addition, gastrin has shown angiogenesis and anti-apoptotic characteristics in several malignancies including gastric cancer 61, 62, 63…”

Section: Gastrin Mediates Its Effects Through the Cholecystokinin-b Rmentioning

confidence: 99%

Gastrin and Gastric Cancer

Smith

Nadella

Osborne

2017

Cellular and Molecular Gastroenterology and Hepatology

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Gastric cancer is the third leading cause of cancer-related mortality worldwide. Despite progress in understanding its development, challenges with treatment remain. Gastrin, a peptide hormone, is trophic for normal gastrointestinal epithelium. Gastrin also has been shown to play an important role in the stimulation of growth of several gastrointestinal cancers including gastric cancer. We sought to review the role of gastrin and its pathway in gastric cancer and its potential as a therapeutic target in the management of gastric cancer. In the normal adult stomach, gastrin is synthesized in the G cells of the antrum; however, gastrin expression also is found in many gastric adenocarcinomas of the stomach corpus. Gastrin’s actions are mediated through the G-protein–coupled receptor cholecystokinin-B (CCK-B) on parietal and enterochromaffin cells of the gastric body. Gastrin blood levels are increased in subjects with type A atrophic gastritis and in those taking high doses of daily proton pump inhibitors for acid reflux disease. In experimental models, proton pump inhibitor–induced hypergastrinemia and infection with Helicobacter pylori increase the risk of gastric cancer. Understanding the gastrin:CCK-B signaling pathway has led to therapeutic strategies to treat gastric cancer by either targeting the CCK-B receptor with small-molecule antagonists or targeting the peptide with immune-based therapies. In this review, we discuss the role of gastrin in gastric adenocarcinoma, and strategies to block its effects to treat those with unresectable gastric cancer.

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Section: Gastrin Mediates Its Effects Through the Cholecystokinin-b Rmentioning

confidence: 99%

Gastrin and Gastric Cancer

Smith

Nadella

Osborne

2017

Cellular and Molecular Gastroenterology and Hepatology

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“…1b), which coordinate the complex gastric physiology by a balanced micromilieu. Embedded within undifferentiated epithelial cells, D cells, G cells and circulating enterochromaffin-like (ECL) cells release regulatory molecules controlling the production of gastric acid by parietal cells [54, 55]. Histamine is released from ECL cells, the hormone gastrin is released by G cells, and the hormone somatostatin is secreted by D cells.…”

Section: Introductionmentioning

confidence: 99%

“…As a negative regulator, somatostatin release is stimulated when the pH in the stomach is too low. Then it blocks acid secretion via direct effects on parietal cells, but also through the inhibition of histamine and gastrin release [54, 55] (Fig. 1b).…”

Section: Introductionmentioning

confidence: 99%

From inflammation to gastric cancer – the importance of Hedgehog/GLI signaling in Helicobacter pylori-induced chronic inflammatory and neoplastic diseases

et al. 2017

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Infections with the human pathogen Helicobacter pylori (H. pylori) are closely associated with the development of inflammatory disorders and neoplastic transformation of the gastric epithelium. Drastic changes in the micromilieu involve a complex network of H. pylori-regulated signal transduction pathways leading to the release of proinflammatory cytokines, gut hormones and a wide range of signaling molecules. Besides controlling embryonic development, the Hedgehog/GLI signaling pathway also plays important roles in epithelial proliferation, differentiation, and regeneration of the gastric physiology, but also in the induction and progression of inflammation and neoplastic transformation in H. pylori infections. Here, we summarize recent findings of H. pylori-associated Hedgehog/GLI signaling in gastric homeostasis, malignant development and the modulation of the gastric tumor microenvironment.

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“…Acid secretion is reduced although the histology of the corpus biopsies remains unaffected. Because of hypoacidity, there may arise the risk for malabsorption of micronutrients (iron, calcium, etc) and vitamin-B12 (24)(25)(26). Differently from LSG, nothing is removed from the abdominal cavity during LRYGB operation where a small pouch created from the proximal part of the stomach is anastomosed to the small bowel leaving 90% of the primary stomach out of food passage.…”

Section: Discussion Discussionmentioning

confidence: 99%

“…A hypoacidic stomach remnant, which is common after LSG, and bypassing of food passage in LRYGB, may impair digestion as well as the absorption of vitamins (eg. vitamin-B12), micronutrients and some pharmaceuticals (24)(25).…”

Section: Discussion Discussionmentioning

confidence: 99%

Serum Gastric Biomarker Levels After Sleeve Gastrectomy and Roux-en-Y Gastric Bypass Operations: A Prospective Study with 1-year Follow-up

Suumann¹,

Sillakivi²,

Riispere³

et al. 2019

SGO

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Objectives:To study the function of the gastric mucosa and acid secretion after bariatric surgery, GastroPanel ® (GP), serum biomarker test was performed in 29 laparoscopic sleeve gastrectomy (LSG) and 28 laparoscopic Roux-en-Y gastric bypass (LRYGB) patients before and after surgery. Methods: Pepsinogen I (PGI), II (PGII), basal fasting gastrin-17 (G17b), stimulated gastrin-17 (G17s) and Helicobacter pylori antibody (HPAB) levels in serum were assayed preoperatively, postoperatively on days 1 and 3, and after 1, 3 and 12 months. Results: The serum levels of PGI, PGII and the PGI/PGII ratio declined significantly in the LSG patients immediately after surgery, and the low levels remained stable throughout the 1-year follow-up period. This was accompanied by a substantially increased output of G17b. In the LRYGB patients, PGI and PGII levels rose markedly during the first 3 postoperative days, thereafter the levels of PGI and PGII, and the PGI/PGII ratio declined significantly. In contrast to LSG, the level of the G17b remained unchanged throughout the whole follow-up period in the LRYGB patients. Excess Weight Loss (%EWL) was 77% and 65% in the LSG and LRYGB groups, respectively. The preoperative biomarker profile did not correlate with %EWL in either of the operative groups. Conclusions: Significant changes do occur in GP biomarker levels following LSG and LRYGB, suggesting reduced functional activity of the gastric corpus with consequent hypoacidity in the gastric remnant, particularly after LSG. Preoperative GP biomarker levels do not predict postoperative %EWL.

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Functional anatomy and physiology of gastric secretion

Abstract: Our understanding of the functional anatomy and physiology of gastric secretion continues to advance. Such knowledge is crucial for improved management of acid-peptic disorders, prevention and management of neoplasia, and the development of novel medications.

Cited by 44 publications

References 38 publications

Gastrin and Gastric Cancer

Gastrin and Gastric Cancer

From inflammation to gastric cancer – the importance of Hedgehog/GLI signaling in Helicobacter pylori-induced chronic inflammatory and neoplastic diseases

Serum Gastric Biomarker Levels After Sleeve Gastrectomy and Roux-en-Y Gastric Bypass Operations: A Prospective Study with 1-year Follow-up

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