Gastric secretion

Schubert, Mitchell L.

doi:10.1097/mog.0000000000000125

Cited by 45 publications

(38 citation statements)

References 45 publications

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“…Gastric acidity has a crucial regulatory factor in gastrin release, and decreased acidity in the stomach stimulates gastrin release [44]. In the past 24-h pH monitoring studies of Japanese volunteers, the median pH in their stomach was not significantly different among the subjects treated with esomeprazole, lansoprazole and rabeprazole (5.7 [3.5–7.2] vs. 5.5 [3.7–7.3] vs. 5.2 [2.5–7.3]) [45].…”

Section: Discussionmentioning

confidence: 99%

Hypergastrinemia in Long-Term Use of Proton Pump Inhibitors

Shiotani¹,

Katsumata²,

Gouda³

et al. 2018

Digestion

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Background/Aim: The use of proton pump inhibitors (PPIs) is known to lead to hypergastrinemia; however, the data in patients with atrophic gastritis is still lacking. The aim of this study was to investigate the effects of long-term PPIs use on the gastrin levels in patients with atrophic gastritis and to determine factors affecting hypergastrinemia in long-term users of PPIs. Methods: Serum Helicobacter pylori IgG, gastrin and pepsinogen levels were measured. Atrophic gastritis was assessed by upper gastrointestinal endoscopies based on the Kimura-Takemoto classification and pepsinogen levels. CYP2C19 polymorphisms were assessed using DNA extracted from peripheral blood. Results: A total number of 382 patients (275 men and 107 women) were enrolled. Median serum gastrin levels were higher in PPI users than in non- users (234 vs. 113 pg/mL, p < 0.001) and in women than in men (252 vs. 155 pg/mL, p = 0.006). Gastrin levels were significantly associated with corpus atrophy only in the subgroup of non-users of PPIs. Multivariate analysis revealed that hypergastrinemia (over 150 pg/mL) was significantly associated with PPI use (OR 5.30; 95% CI 3.32–8.47), women (OR 2.22; 95% CI 1.33–3.72) and corpus atrophy (OR 1.82; 95% CI 1.14–2.90). Conclusion: PPI use, women and corpus atrophy were risk factors for hypergastrinemia. Gender, but not corpus atrophy, affected the gastrin levels in long-term users of PPIs.

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Section: Discussionmentioning

confidence: 99%

Hypergastrinemia in Long-Term Use of Proton Pump Inhibitors

Shiotani¹,

Katsumata²,

Gouda³

et al. 2018

Digestion

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“…Gastric acid activates pepsinogen, denatures proteins and protects against pathogens (Martinsen et al, 2005; Beasley et al, 2015) (Figure 1A). Hypo-or achlorhydria (low or absent gastric acid, respectively) can result from a variety of conditions, including atrophic gastritis (Strickland and Mackay, 1973), gastrectomy (Hoya et al, 2009), acid suppression therapy (e.g., proton pump inhibitors, antacid medication) (Schubert, 2014) and Helicobacter pylori infection (Schubert, 2014). Though the lowered gastric acid production increases infection risk (Martinsen et al, 2005), the consequences of low acidity in protein digestion remain poorly understood.…”

Section: Consumers Differ In Digestive Capacitymentioning

confidence: 99%

Personalizing protein nourishment

Dallas

Sanctuary

et al. 2017

Critical Reviews in Food Science and Nutrition

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Proteins are not equally digestible—their proteolytic susceptibility varies by their source and processing method. Incomplete digestion increases colonic microbial protein fermentation (putrefaction), which produces toxic metabolites that can induce inflammation in vitro and have been associated with inflammation in vivo. Individual humans differ in protein digestive capacity based on phenotypes, particularly disease states. To avoid putrefaction-induced intestinal inflammation, protein sources and processing methods must be tailored to the consumer’s digestive capacity. This review explores how food processing techniques alter protein digestibility and examines how physiological conditions alter digestive capacity. Possible solutions to improving digestive function or matching low digestive capacity with more digestible protein sources are explored. Beyond the ileal digestibility measurements of protein digestibility, less invasive, quicker and cheaper techniques for monitoring the extent of protein digestion and fermentation are needed to personalize protein nourishment. Biomarkers of protein digestive capacity and efficiency can be identified with the toolsets of peptidomics, metabolomics, microbial sequencing and multiplexed protein analysis of fecal and urine samples. By monitoring individual protein digestive function, the protein component of diets can be tailored via protein source and processing selection to match individual needs to minimize colonic putrefaction and, thus, optimize gut health.

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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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Gastric secretion

Abstract: Our understanding of the regulation of gastric acid secretion continues to advance. Such knowledge is crucial for the management of acid-peptic disorders and the development of novel medications, such as cholecystokinin-2 receptor antagonists.

Cited by 45 publications

References 45 publications

Hypergastrinemia in Long-Term Use of Proton Pump Inhibitors

Hypergastrinemia in Long-Term Use of Proton Pump Inhibitors

Personalizing protein nourishment

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

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