Additionally, exogenous H 2 S has been shown to protect the gastric mucosa on different model of experimentally induced gastric ulcer in rats [7-9]. This phase is initiated by entry of food into the duodenum and contributes about 10% of total acid secretion. It is not fully clear how this phase is regulated but may be due to small amounts of gastrin secretion by the duodenal small intestine mucosa. Secretion of stomach acid can be divided into three phases which correspond to the different stages of food ingestion.
There is a decline in acid output in elderly patients who develop chronic gastritis, but acid output is otherwise maintained throughout life. Fig 1 – Diagram showing the production of Hydrochloric acid within the stomach.
The enzyme activity and mRNA expression of CSE have been shown in the rat stomach . Recently, we have shown that pharmacological inhibition of CSE by preadministration of PAG leads to an increase in the gastric acid output in response to distention compared to corresponding control . As shown in Figure 1, the results of present study were also confirmed by the previous findings that suggest that the CSE activity and H 2 S production increase concomitant of gastric acid stimulation and decrease the acid output in response to gastric distention. According to Figure 5, mRNA expression of H + /K + -ATPase Î±-subunit in PAG-treated rats significantly increased as compared to control group.
Chemical stimuli (i.e., partially digested proteins, caffeine) directly activate G cells (enteroendocrine cells) that are located in the pyloric region of the stomach to secrete gastrin; this in turn stimulates the gastric glands to secrete gastric juice. The cephalic phase causes ECL cells to secrete histamine and increase HCl acid in the stomach. There will also be an influence on G cells to increase gastrin circulation.
This study investigated whether gastric and oral TAS2Rs contribute to the regulation of caffeine-induced mechanisms of GAS in humans. To study this hypothesis, the effect of caffeine on GAS was investigated in a human intervention trial, taking into account taste receptor activation in the mouth and the stomach. The underlying gastric mechanisms were studied by TAS2R expression analysis and by means of the validated HGT-1 cell culture model, which maintains the relevant characteristics of human parietal cells (28, 29).
- Delta reacidification time was calculated by substraction of the reacidification time of the water or empty capsule control from the reacidification time after the treatment.
- exchangers, which are also expressed in the parietal cell, may function to maintain pH homeostasis (8) rather than playing a direct role in support of acid secretion.
- This endless increase of PPI utilization has created an important problem for many regulatory authorities in terms of increased costs and greater potential risk of adverse events.
- In epithelial cells of the inner ear, pancreas, and airways it interacts with IsK to conduct a voltage-gated and slowly activating K+ current.
For instance, studies in vitro have shown that NO stimulates secretion of gastric acid in the mouse[17, 18] and bullfrog. In addition, similar results have been obtained in dogs . However, other investigations have shown that NO inhibits gastric acid secretion in the rat [13, 14], in gastric glands isolated from rabbits , and in mucosa from toads . Studies of humans have provided data indicating that NO can both inhibit and augment intragastric pH [20, 21], but it is not yet known how this compound participates in gastric acid secretion in humans.
Below pH of 2, stomach acid inhibits the parietal cells and G cells; this is a negative feedback loop that winds down the gastric phase as the need for pepsin and HCl declines. In Zollinger-Ellison syndrome and hypercalcemia, there are increased gastrin levels, leading to excess gastric acid production, which can cause gastric ulcers.
We demonstrated here that the bitter-masking agent HED reduced the stimulatory effect of caffeine on proton secretion in healthy subjects and in HGT-1 cells. As TAS2R43 is the only one of the five TAS2Rs that can be activated by caffeine and antagonized by HED, we also performed a CRISPR-Cas9 approach to knock out TAS2R43 in HGT-1 cells.
Beyond their chemosensory function, extraoral TAS2Rs are involved in nonsensory processes to expel or neutralize toxins in the upper and lower airways as well as in the gastrointestinal tract (19). Furthermore, the TAS2R pathway in the gut is involved in the regulation of food intake, digestion, and satiation (15, 16, 20, 21). Whereas, in the stomach, the endocrine effect of bitter substances on ghrelin secretion has been well described (20), a bitter compound-mediated exocrine function on acid production in parietal cells had not yet been discovered to our knowledge. Parietal cells can be activated by histamine or acetylcholine binding to their cognate histamine H2 or acetylcholine M3 receptors (22).
Since NO has been shown to inhibit gastric acid secretion in rabbit, human and rat [12-14], the present study aimed to elucidate the possible mechanism of the inhibitory effect of NaHS, a H 2 S donor, on gastric acid secretion in rats and to determine whether this effect is related to nitric oxide. This phase is initiated by entry of food into the stomach and contributes about 70% of total acid secretion.