Postulated Physiological and Pathophysiological Roles on Motility
Edwin E. Daniel in Neuropeptide Function in the Gastrointestinal Tract, 2019
Gastrin is a potent stimulator of gastric acid secretion. Its role in the regulation of gastrointestinal motility is far less characterized. Excessive secretion of gastrin can be observed due to a gastrinoma, a gastrin-producing tumor, or as a consequence of reduced acid secretion caused by Billroth II surgery, atrophic gastritis, or drugs (H2 blockers or omeprazol). No specific motility changes in these hypergastrinemia conditions have been reported, and the diarrhea observed in gastrinoma patients probably is primarily due to the changes in the secretory responses and, to a minor extent, to motility changes. The possible physiological role in the regulation of antral motility and in the maintenance of the basal lower esophageal sphincter pressure awaits further confirmation with new selective gastrin receptor antagonists.
Gastrointestinal Function and Toxicology in Canines
Shayne C. Gad in Toxicology of the Gastrointestinal Tract, 2018
The hormone gastrin is produced in two different equally important forms, one a 34 amino acid polypeptide called G-34 and the other a 17 amino acid polypeptide referred to as G-17. The G-17 form is the more abundantly produced substance. Gastrin is produced by G or gastrin cells, which reside in the pyloric glands of the distal stomach. As protein enters the antral portion of the stomach, its presence directly evokes a stimulatory response from the gastrin cells of the pyloric glands, resulting in the release of gastrin into the lumen of the stomach. The mixing of the gastric luminal contents promotes the interaction of gastrin with the enterochromaffin cells in the body of the stomach and histamine is released from the enterochromaffin cells. This histamine in turn stimulates the production of hydrochloric acid from parietal cells.
Stomach and duodenum
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie in Bailey & Love's Short Practice of Surgery, 2018
The secretion of gastric acid and pepsin tends to run in parallel, although the understanding of the mechanisms of gastric acid secretion is considerably greater than that of pepsin. Numerous factors are involved to some degree in the production of gastric acid. These include neurotransmitters, neuropeptides and peptide hormones. This complexity need not detract from the fact that there are basic principles that are relatively easily understood (Figure63.4). Hydrogen ions are produced by the parietal cell by the proton pump. Although numerous factors can act on the parietal cell, the most important of these is histamine, which acts via the H2-receptor. Histamine is produced, in turn, by the ECL cells of the stomach and acts in a paracrine (local) fashion on the parietal cells. These relationships explain why proton pump inhibitors can abolish gastric acid secretion, as they act on the final common pathway - hydrogen ion secretion. H2-receptor antagonists have profound effects on gastric acid secretion, but this is not insurmountable (Figure63.4). The ECL cell produces histamine in response to a number of stimuli that include the vagus nerve and gastrin. Gastrin is released by the G cells in response to the presence of the food in the stomach. The production of gastrin is inhibited by acid, creating a negative feedback loop. Various other peptides, including secretin, inhibit gastric acid secretion.
Decreased anti-parietal cell antibody titer in the advanced phase of autoimmune gastritis
Published in Scandinavian Journal of Gastroenterology, 2022
Toshihiro Nishizawa, Hidenobu Watanabe, Shuntaro Yoshida, Akira Toyoshima, Yosuke Kataoka, Takamitsu Kanazawa, Naoto Yoshizawa, Hirotoshi Ebinuma, Hidekazu Suzuki, Osamu Toyoshima
During the study period, 50 patients were pathologically diagnosed with AIG. Six patients were not tested for APCA and were thus excluded. Ultimately, we included 44 AIG patients with APCA results in this study. The characteristics of the 44 patients are shown in Table 1. There were two patients in the early phase, 11 in the florid phase, and 31 in the end phase. APCA-positive rates were 100% in the early phase, 90.9% in the florid phase, and 90.3% in the end phase. The mean APCA titer was 480 ± 226 U in the early phase, 220 ± 235 U in the florid phase, and 150 ± 152 U in the end phase. There was a stepwise decrease in the APCA titer from the early phase to the end phase. The mean APCA titer for the end phase was significantly lower than that of the early phase or florid phase. The mean serum gastrin level was 2565 ± 854 pg/ml in the early phase, 2685 ± 2129 pg/ml in the florid phase, and 2810 ± 1619 pg/ml in the end phase. The mean serum gastrin level in the end phase was significantly higher than that in the early phase or florid phase. Representative histological images of AIG are shown in Figures 1 and 2 for the early and end phases, respectively.
Gastrin secretion in normal subjects and diabetes patients is inhibited by glucagon-like peptide 1: a role in the gastric side effects of GLP-1-derived drugs?
Published in Scandinavian Journal of Gastroenterology, 2019
Jens F. Rehfeld, Filip K. Knop, Meena Asmar
This study shows that GLP-1 in pharmacological doses inhibits the gastrin-response to food, both in normal subjects and in diabetes patients (Figure 1, Table 1). Gastrin is the classical hormonal regulator of the functions of the stomach. Hence, gastrin is the decisive stimulator of gastric acid and enzyme secretion during food ingestion. In addition, gastrin also has trophic effects on the gastric mucosa and maintain mucosal integrity by stimulation cell proliferation, migration and angiogenesis. Finally, gastrin may influence the motility of the stomach [22], although this has been less well studied in man. As shown in knock-out mice, lack of gastrin inhibits the acid-producing machinery; and permanent lack of acid subsequently leads to intestinal metaplasia and tumor development in the stomach [23,24]. Thus, long-term suppression of gastrin secretion may interfere with digestion and the function of the stomach, although translation of results from rodents to man requires some caution. Nevertheless, the randomized and controlled trials [10–16] have all shown that GLP-1-derived drugs have adverse gastrointestinal side effects including dyspepsia, nausea and upper abdominal pain, which are likely to originate from a malfunctioning stomach. The pronounced suppression of food-stimulated gastrin secretion in diabetes patients (Figure 1) in itself suggests that gastric functions deserve attention – including endoscopy – during long-term therapy with GLP-1-derived drugs. In this respect, especially patients with type 2 diabetes come into focus.
Cardiac remodeling in obesity and after bariatric and metabolic surgery; is there a role for gastro-intestinal hormones?
Published in Expert Review of Cardiovascular Therapy, 2019
Elijah Sanches, Marieke Timmermans, Besir Topal, Alper Celik, Magnus Sundbom, Rui Ribeiro, Chetan Parmar, Surendra Ugale, Monika Proczko, Pieter S. Stepaniak, Juan Pujol Rafols, Kamal Mahawar, Marc P. Buise, Aleksandr Neimark, Rich Severin, Sjaak Pouwels
The G cells in the duodenum and the pyloric antrum of the stomach mainly produce gastrin, after modifying its precursor preprogastrin. Its primary function is stimulating acid secretion by releasing histamine from enterochromaffin-like cells [222]. Historically, it was the first gut hormone to be studied in bariatric surgery in 1975 [223,224]. Earlier studies showed an increase of gastrin after small bowel resection [223,224]. A small number of studies is available studying the effects of gastrin after bariatric surgery of which a few studies reveal an increase in basal and postprandial levels mainly in jejunoileal bypass [225,226], the vast majority of bypass procedures reveal either no significant change or a decrease of both circulating and post-prandial levels [143–145,147,151,223–225,227]. In gastric banding, the study of Shak et al. [167] showed no significant postoperative changes. In VBG surgery an increase was seen in both basal and postprandial levels [151,228]. It is postulated that gastric pouch ulcers might be related to the increase of gastrin seen after VBG [229].
Related Knowledge Centers
- G Cell
- Gastric Acid
- Pancreas
- Parietal Cell
- Peptide
- Peptide Hormone
- Pylorus
- Stomach
- Duodenum
- Cholecystokinin B Receptor