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Physiological Reviews Apr 2020Parietal cells are responsible for gastric acid secretion, which aids in the digestion of food, absorption of minerals, and control of harmful bacteria. However, a fine... (Review)
Review
Parietal cells are responsible for gastric acid secretion, which aids in the digestion of food, absorption of minerals, and control of harmful bacteria. However, a fine balance of activators and inhibitors of parietal cell-mediated acid secretion is required to ensure proper digestion of food, while preventing damage to the gastric and duodenal mucosa. As a result, parietal cell secretion is highly regulated through numerous mechanisms including the vagus nerve, gastrin, histamine, ghrelin, somatostatin, glucagon-like peptide 1, and other agonists and antagonists. The tight regulation of parietal cells ensures the proper secretion of HCl. The H-K-ATPase enzyme expressed in parietal cells regulates the exchange of cytoplasmic H for extracellular K. The H secreted into the gastric lumen by the H-K-ATPase combines with luminal Cl to form gastric acid, HCl. Inhibition of the H-K-ATPase is the most efficacious method of preventing harmful gastric acid secretion. Proton pump inhibitors and potassium competitive acid blockers are widely used therapeutically to inhibit acid secretion. Stimulated delivery of the H-K-ATPase to the parietal cell apical surface requires the fusion of intracellular tubulovesicles with the overlying secretory canaliculus, a process that represents the most prominent example of apical membrane recycling. In addition to their unique ability to secrete gastric acid, parietal cells also play an important role in gastric mucosal homeostasis through the secretion of multiple growth factor molecules. The gastric parietal cell therefore plays multiple roles in gastric secretion and protection as well as coordination of physiological repair.
Topics: Animals; Cell Shape; Gastric Acid; H(+)-K(+)-Exchanging ATPase; Homeostasis; Humans; Parietal Cells, Gastric; Potassium; Proton Pump Inhibitors; Secretory Pathway; Signal Transduction
PubMed: 31670611
DOI: 10.1152/physrev.00016.2019 -
Cleveland Clinic Journal of Medicine Nov 2003Gastroesophageal reflux disease (GERD) is a specific clinical entity defined by the occurrence of gastroesophageal reflux through the lower esophageal sphincter (LES)... (Review)
Review
Gastroesophageal reflux disease (GERD) is a specific clinical entity defined by the occurrence of gastroesophageal reflux through the lower esophageal sphincter (LES) into the esophagus or oropharynx to cause symptoms, injury to esophageal tissue, or both. The pathophysiology of GERD is complex and not completely understood. An abnormal LES pressure and increased reflux during transient LES relaxations are believed to be key etiologic factors. Prolonged exposure of the esophagus to acid is another. Heartburn and acid regurgitation are the most common symptoms of GERD, although pathologic reflux can result in a wide variety of clinical presentations. GERD is typically chronic, and while it is generally nonprogressive, some cases are associated with development of complications of increasing severity and significance.
Topics: Esophagogastric Junction; Female; Gastric Acid; Gastroesophageal Reflux; Humans; Hydrogen-Ion Concentration; Male; Manometry; Prognosis; Risk Factors; Severity of Illness Index
PubMed: 14705378
DOI: 10.3949/ccjm.70.suppl_5.s4 -
Digestive Diseases (Basel, Switzerland) 2020Less than 2 centuries have elapsed since the identification of hydrochloric acid in the stomach. The clarification of the molecular mechanisms allowed the effective... (Review)
Review
Less than 2 centuries have elapsed since the identification of hydrochloric acid in the stomach. The clarification of the molecular mechanisms allowed the effective therapeutic suppression of gastric acid secretion. The spectacular advances in the treatment of acid-related disorders represent a synthesis of the contributions of several brilliant pharmacologists, basic scientists, and clinical physicians. Effective gastric acid suppressive therapy has dramatically improved the therapy and outcome of acid-related disorders. The introduction of proton pump inhibitors (PPIs) in clinical practice has significantly changed the medical management of upper gastrointestinal disorders. PPIs represent the "gold-standard" therapy in acid-related disorders. However, some challenges persist in the therapy of acid related diseases, including management of patients who respond inadequately to PPI therapy, more effective gastroprotection, or more powerful antisecretory treatment for the eradication of Helicobacter pylori infection. New antisecretory drugs are currently being developed and investigated to further provide a more effective and profound gastric acid secretion inhibition. The major advance has been the development of acid pump -antagonists, the potassium channel acid blocking drugs (-P-CABs). Long-term studies comparing P-CABs with PPIs will help to define the exact place and safety profile of this class of drug in the management of acid-related disorders.
Topics: Drug Development; Gastric Acid; Gastrointestinal Agents; Histamine Antagonists; Humans; Potassium Channel Blockers; Proton Pump Inhibitors
PubMed: 31846972
DOI: 10.1159/000505204 -
British Medical Journal (Clinical... May 1985During a study of gastric secretion four out of six previously healthy subjects developed hypochlorhydria after a transient illness with nausea, vomiting, and abdominal... (Clinical Trial)
Clinical Trial
During a study of gastric secretion four out of six previously healthy subjects developed hypochlorhydria after a transient illness with nausea, vomiting, and abdominal pain. Mean basal and peak acid outputs were 0 and 2.3 mmol (84 mg)/h one month after the onset of illness and 1.5 and 27.0 mmol/h (55 and 984 mg/h) at eight months' follow up. Two of the subjects were followed up at 18 months, when mean basal and peak acid outputs were 3.9 and 33.5 mmol/h (142 and 1221 mg/h). No endoscopic abnormality was seen at one and eight months, but biopsies showed active superficial gastritis, which resolved in one subject and became chronic in two. Schilling tests performed in three subjects at eight months showed diminished retention of vitamin B12. During hypochlorhydria a 24 hour intragastric analysis was performed for total and nitrate reducing bacteria, pH, and concentrations of nitrite and total and stable N-nitroso compounds. Of the 48 samples of gastric juice examined, 47 had bacterial growth of more than 10(6) organisms/ml and 46 had growth of nitrate reducing bacteria of more than 10(5) organisms/ml. Mean intragastric nitrite concentrations were 10 times higher than in a group of eight healthy controls. Both mean total and mean stable N-nitroso compound concentrations, however, were not appreciably different from those in controls. Although community transmission was a possibility, serological screening and electron microscopy of gastric biopsy specimens failed to show an infective cause. Transmission of an unidentified enteric pathogen via a contaminated pH electrode was therefore suspected. Thus gastric juice should not be returned to the stomach after contact with a contaminated glass electrode as this is a possible cause of atrophic gastritis.
Topics: Achlorhydria; Disease Outbreaks; Gastric Acid; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastritis; Humans; Nitrites; Secretory Rate
PubMed: 3922503
DOI: 10.1136/bmj.290.6479.1383 -
World Journal of Gastroenterology Nov 2020Proton pump inhibitors strongly inhibit gastric acid production, but digestion problems do not generally arise. We can intake almost ordinary food even after total... (Review)
Review
Proton pump inhibitors strongly inhibit gastric acid production, but digestion problems do not generally arise. We can intake almost ordinary food even after total gastrectomy. Small intestine itself can digest and absorb food using various digestive enzymes without digestion in the stomach. The pH level of gastric acid in humans is much lower than that of most animals, and very close to that of carrion-eating animals called scavengers. It is assumed that ancient humans became bipedal approximately 4 million years ago. It was difficult for humans, who just started unstable bipedal locomotion, to catch quadrupedal-walking animals that can move faster, without special hunting tools. They may have eaten remaining carcasses, which is mainly the leftovers of carnivora species, as animal-derived food. The benefit to produce a volume of gastric acid for humans is carrion eating, in which disinfection by gastric acid is important. Humans produce a high concentration of gastric acid to enable consumption of a diet containing some bacteria and support this lifestyle by consuming significant energy to protect themselves from gastric acid. Now, the opportunity for strong deleterious bacteria to enter the gastrointestinal tract has decreased because of the organized clean environment. If this hygienic environment is maintained for a long time, our gastric acid level must be decreased gradually.
Topics: Animals; Diet; Gastric Acid; Gastrointestinal Tract; Humans; Proton Pump Inhibitors; Stomach
PubMed: 33268958
DOI: 10.3748/wjg.v26.i43.6706 -
Nature Reviews. Gastroenterology &... May 2018Subjected to countless daily injuries, the stomach still functions as a remarkably efficient digestive organ and microbial filter. In this Review, we follow the lead of... (Review)
Review
Subjected to countless daily injuries, the stomach still functions as a remarkably efficient digestive organ and microbial filter. In this Review, we follow the lead of the earliest gastroenterologists who were fascinated by the antiseptic and digestive powers of gastric secretions. We propose that it is easiest to understand how the stomach responds to injury by stressing the central role of the most important gastric secretion, acid. The stomach follows two basic patterns of adaptation. The superficial response is a pattern whereby the surface epithelial cells migrate and rapidly proliferate to repair erosions induced by acid or other irritants. The stomach can also adapt through a glandular response when the source of acid is lost or compromised (that is, the process of oxyntic atrophy). We primarily review the mechanisms governing the glandular response, which is characterized by a metaplastic change in cellular differentiation known as spasmolytic polypeptide-expressing metaplasia (SPEM). We propose that the stomach, like other organs, exhibits marked cellular plasticity: the glandular response involves reprogramming mature cells to serve as auxiliary stem cells that replace lost cells. Unfortunately, such plasticity might mean that the gastric epithelium undergoes cycles of differentiation and de-differentiation that increase the risk of accumulating cancer-predisposing mutations.
Topics: Animals; Cell Plasticity; Cellular Reprogramming; Gastric Acid; Gastric Mucosa; Humans; Stomach; Stomach Neoplasms
PubMed: 29463907
DOI: 10.1038/nrgastro.2018.5 -
Applied Microbiology and Biotechnology Jan 2020Microorganisms encounter acid stress during multiple bioprocesses. Microbial species have therefore developed a variety of resistance mechanisms. The damage caused by... (Review)
Review
Microorganisms encounter acid stress during multiple bioprocesses. Microbial species have therefore developed a variety of resistance mechanisms. The damage caused by acidic environments is mitigated through the maintenance of pH homeostasis, cell membrane integrity and fluidity, metabolic regulation, and macromolecule repair. The acid tolerance mechanisms can be used to protect probiotics against gastric acids during the process of food intake, and can enhance the biosynthesis of organic acids. The combination of systems and synthetic biology technologies offers new and wide prospects for the industrial applications of microbial acid tolerance mechanisms. In this review, we summarize acid stress response mechanisms of microbial cells, illustrate the application of microbial acid tolerance in industry, and prospect the introduction of systems and synthetic biology to further explore the acid tolerance mechanisms and construct a microbial cell factory for valuable chemicals.
Topics: Acids; Bacteria; Gastric Acid; Hydrogen-Ion Concentration; Industrial Microbiology; Metabolic Engineering; Probiotics; Stress, Physiological; Synthetic Biology; Systems Biology
PubMed: 31773206
DOI: 10.1007/s00253-019-10226-1 -
Brazilian Dental Journal 2022The purpose of this in vitro study was to evaluate the effect of gastric acid on the surface roughness and biofilm formation of bulk-fill composite resins. Twenty-seven...
The purpose of this in vitro study was to evaluate the effect of gastric acid on the surface roughness and biofilm formation of bulk-fill composite resins. Twenty-seven samples of each composite resin were obtained: G1: Filtek Z250 XT (Z250), G2: Filtek Bulk Fill (FTK), G3: Tetric N-Ceram Bulk Fill (TTC), and G4: Aura Bulk Fill (AUR). The samples were quantitatively analyzed for surface roughness (Ra) using a roughness tester (n=15) and for biofilm formation (Cn) by the counting of colony-forming units (CFUs/mL) (n=9) in three different moments: after polishing (Ra0 and Cn0), after gastric acid immersion (Ra1 and Cn1), and after gastric acid and simulated tooth brushing (Ra2 and Cn2). Qualitative analysis through surface topography (n=3) was evaluated by scanning electron microscopy (SEM). Ra values were subjected to two-way repeated measures ANOVA, followed by Tukey's test. Cn values were subjected to Kruskal-Wallis analysis, followed by multiple comparisons analysis (α=0.05). Z250 and FTK showed significant increases in surface roughness at Ra1. There were fewer CFUs/mL on TTC and AUR in relation to those of Z250 and FTK for Cn0, Cn1 and Cn2. The SEM images showed that gastric acid increased the formation of cracks, exposure of fillers and micro cavities for all composite resins. After tooth brushing, the topographical changes were more evident but did not influence biofilm formation. The gastric acid promoted both degradation of the surfaces and bacterial adhesion for all composite resins.
Topics: Bacterial Adhesion; Gastric Acid; Composite Resins
PubMed: 36477970
DOI: 10.1590/0103-6440202205140 -
Digestion 2008Evidence from comparative anatomy and physiology studies indicates that gastric acid secretion developed during the evolution of vertebrates approximately 350 million... (Review)
Review
Evidence from comparative anatomy and physiology studies indicates that gastric acid secretion developed during the evolution of vertebrates approximately 350 million years ago. The cellular mechanisms that produce gastric acid have been conserved over the millennia and therefore proton pump inhibitors have pharmacological effects in almost all relevant species. These observations suggest that gastric acid provides an important selective advantage; however, in modern-day humans the need for gastric acid can be questioned in light of the widespread use of safe and effective pharmacologic acid suppression. The Kandahar Working Group addressed questions concerning the need, production and effects of gastric acid, specifically: (1) motility in the upper gastrointestinal (GI) tract; (2) neuroendocrine factors; (3) digestive and mucosal processes; (4) microbiology, and (5) central processes and psychological involvement. We addressed each topic with the individual models available to answer our questions including animal versus human studies, pharmacologic, surgical as well as pathophysiologic states of acid suppression.
Topics: Amyloid; Animals; Calcium; Epithelium; Feeding Behavior; Gastric Acid; Gastric Emptying; Gastritis; Gastroenteritis; Gastrointestinal Motility; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Absorption; Iron, Dietary; Islet Amyloid Polypeptide; Satiation; Secretin; Somatostatin; Stomach; Stress, Psychological
PubMed: 18594142
DOI: 10.1159/000142726 -
Medicina (Kaunas, Lithuania) Aug 2022Background and Objectives: The aim of this in vitro study was to evaluate the effect of simulated gastric acid associated with toothbrushing on the surface condition of...
Background and Objectives: The aim of this in vitro study was to evaluate the effect of simulated gastric acid associated with toothbrushing on the surface condition of three resin-modified glass-ionomer cements (RMGIC). Materials and Methods: One hundred and sixty samples of each material were obtained and included in three study groups according to the tested material: Group I (Ionolux, VOCO GmbH, Cuxhaven, Germany); Group II (Vitremer, 3 M-ESPE, St. Paul, MN, USA); and Group III (Fuji II LC, GC Corporation, Tokyo, Japan). The samples were submersed in hydrochloric acid 0.01 M (pH 3.8) for 3 h and exposed to a toothbrushing procedure at a frequency of 10,000 cycles with medium and hard bristles immediately or 30 min after the acid attack. Profilometric measurements were performed by using a non-contact profilometer (Dektak XT, Bruker, Billerica, MA, USA) in order to assess the surface roughness. ANOVA and Bonferroni post hoc tests were used for the statistical analysis at a significance level of p < 0.05. Results: Exposure of RMGICs to the erosive effect of hydrochloric acid in association with toothbrushing 30 min after the chemical attack increased the surface roughness of all three RMGICs. Exposure of the three tested materials exclusively to the action of hydrochloric acid did not affect the surface roughness. Conclusions: One year of hydrochloric acid challenge associated with one year of toothbrushing with medium-hardness bristles performed 30 min after the acid attack increase the surface roughness of two of the three types of RMGIC tested (Ionolux and Fuji II LC).
Topics: Gastric Acid; Glass Ionomer Cements; Humans; Hydrochloric Acid; Materials Testing; Surface Properties; Toothbrushing
PubMed: 36143826
DOI: 10.3390/medicina58091149