Raguse (Charité, Berlin, Germany). Whereas primers for TAS2Rs 8, 9, and 60 could be verified, TAS2R45 was not detected. For TAS2R45, high-frequency copy-number variants are known, and some people do not possess the tested variant of the mRNA for this gene (44). TAS2R46 could not be detected in the second human biopsy sample.
Serum gastrin concentrations rose significantly whenever intragastric pH was raised. Serum gastrin also rose after MgCl2, AlCl3, and CaCl2 with a pH of 2, when intragastric pH was not significantly altered. This rise, however, was significantly smaller than after administration of the antacids, except in the MgCl2-Mg(OH)2 and in the CaCl2 pH 10-CaCO3 groups. No significant rise of serum gastrin levels was observed after BaSO4.
Enterochromaffin-like (ECL) cells are endocrine/paracrine cells that are numerous in the acid-producing part of the stomach in many species. In the rat, they occur predominantly in the basal half of the oxyntic mucosa and produce and store histamine. The ECL cells have an unknown function and do not seem to respond to stimuli from the gastric lumen. They are activated by circulating gastrin and by vagal excitation.
Endothelial nitric oxide synthase (eNOS) has previously been detected in the glandular part of the human gastric mucosa. Furthermore, nitric oxide (NO) has been shown to influence gastric secretion in various animal models. The present study was conducted to investigate the influence of exogenously and endogenously derived NO on histamine- and cAMP-stimulated gastric acid secretion in isolated human oxyntic glands. Parietal cells (also called oxyntic cells) are the stomach epithelium cells which secrete gastric acid. These results indicate that sst2 is the main subtype whereby endogenous somatostatin suppresses gastric acid secretion through inhibition of gastrin action.
The responses were similar in magnitude, or even more pronounced, compared with those elicited by histamine, a major activator of proton secretion in parietal cells (10). These responses to bitter compounds indicate that several TAS2Rs could be activated in HGT-1 cells. Treatment of HGT-1 cells with 0.3-3,000 µM caffeine increased proton secretion, with 3,000 µM caffeine showing the highest effect (Fig. S6 A and B). The bitter-masking compounds HED and eriodictyol (ED), which have been described to reduce the bitter taste of caffeine in human sensory panels (33, 34), also reduced the caffeine-evoked proton secretion in HGT-1 cells (Fig. 4B and Fig. S6C).
Lansoprazole (both doses) as well as omeprazole raised the plasma gastrin levels about 11-fold 2 h after dosing and 8-to 10-fold 24 h after dosing, reflecting complete (2 h) and 70-80% (24 h) reductions of gastric acid secretion. Administration of either drug for 10 weeks increased the weight of the stomach and the oxyntic mucosa. The oxyntic mucosal histidine decarboxylase activity, histamine concentration and ECL cell density were increased to the same extent in the rats given either of the two lansoprazole doses or omeprazole.
The secretion of gastric acid is an important inhibitor of gastrin release. If the pH of the antral contents falls below 2.5, gastrin is not released.
These findings were corroborated by immunohistochemical detection of TAS2R10 and transducin in different gastric cell types for which useful antisera were available. So far, to our knowledge, only one validated antibody against human TAS2R38 (38) is known. Neither caffeine nor HED bind to TAS2R38.
(2012 ) Identification of beer bitter acids regulating mechanisms of gastric acid secretion . (1975 ) Gastric acid secretion and lower-esophageal-sphincter pressure in response to coffee and caffeine . As TAS2R10 was highly expressed in parietal cells, as detected by immunohistological staining, we focused on the cellular mechanisms in HGT-1 cells, which exhibit the characteristics of parietal cells (28, 29). Nevertheless, we cannot exclude that other cell types or gastrointestinal hormones may have contributed to the detected effects in the human intervention study.
In nonulcer subjects, gastrin response was smaller than in the duodenal ulcer patients. The results suggest that administration of nonbuffering Mg-, Al-, and Ca-chlorides leads to elevated serum gastrin levels in duodenal ulcer patients; rising intragastric pH, however, exerts an additional serum gastrin response.
Acutely induced gastric ulcers or erosions such as Shay ulcers, water-immersion stress-, indomethacin-, aspirin-, or prednisolone-induced erosions were all markedly inhibited by oral or intraduodenal administration of 10-100 mg/kg of omeprazole. The development of duodenal ulcers and gastric erosions caused by mepirizole was also potently inhibited by omeprazole at 3-10 mg/kg given orally. Repeated administration of omeprazole, 200 mg/kg/day in two divided doses for 14 days, significantly accelerated the spontaneous healing of acetic acid-induced gastric ulcers. The mechanism by which omeprazole inhibits the development of acute ulcers and accelerates healing of preexisting ulcers appears to be mainly due to its potent and long-lasting antisecretory activity. The antisecretory and antiulcer activities of omeprazole are equal to or exceed those of cimetidine, both in the maximum inhibitory response and ED50 values.
Therefore, the tonic activity of α-gustducin regulates taste cell responsivity. Transducin, a similar G protein also present in taste cells, can replace the function of α-gustducin (25, 26). TAS2R-expressing cells in the gastrointestinal tract have been reported to coexpress the downstream taste signaling components, suggesting that similar signal transduction pathways could also mediate gastrointestinal physiology (27). However, the detailed signal transduction pathways in extraoral chemosensitive cells are yet unknown.
The endocrine cell populations in the antrum usually differ from those in the oxyntic mucosa. Gastrin cells are found in the antrum and respond readily to stimuli from the gastric lumen, such as changes in the pH and the presence of food. In order to study the functional control of the antral gastrin cell, rats were subjected to different kinds of surgery.