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StomachGastric Secretions, Motility, Digestion and Vomiting
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Gastric secretion occurs in three phases: cephalic, gastric and intestinal. The cephalic phase is initiated by the thought, sight, taste and smell of food mediated via the vagus. Vagal stimulation activates enteric nerves to release gastrin-releasing peptide (GRP) and acetylcholine. GRP released near the G cells stimulates the secretion of gastrin into blood to activate parietal and chief cells. About 20%–30% of gastric secretions (HCl, gastrin and pepsinogen) released during a meal may occur as a result of the cephalic phase.
The liver, gallbladder and pancreas
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Dina G. Tiniakos, Alastair D. Burt
Gastrinomas are NETs that produce gastrin. Gastrin is normally produced only by G-cells in the stomach and duodenum. Most gastrinomas occur in the submucosa of the duodenum or the gastric antrum, but the pancreas is the most common site for an ectopic gastrinoma. Gastrinomas are associated with the Zollinger–Ellison syndrome in which persistent hypersecretion of acid gastric juice causes duodenal and even jejunal peptic ulceration (see Chapter 10, Case History 10.2). Most pancreatic gastrinomas are malignant.
Postulated Physiological and Pathophysiological Roles on Motility
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
Hans-Dieter Allescher, Sultan Ahmad
In dogs and other mammalian species the majority of G cells are localized in the antrum,18 whereas in man there are also many G cells in the proximal duodenum.19,20 Gastrin is produced from a precursor peptide by enzymatic cleavage and, like CCK, several molecular forms can be extracted and measured in the plasma. The antral cells contain mainly the 17-amino-acid form, G-17, whereas the duodenum contains mainly the N-terminally extended form, G-34 (big-gastrin).21 G-17 and G-34 are of similar potency, but G-17 is degraded more rapidly than the more stable G-34. Consequently, in the fasted state the majority of serum gastrin is G-34 (two thirds of total gastrin), whereas after gastrin release by a meal the amounts of G-17 and G-34 are almost equal.22–25
Long-term changes in serum gastrin levels during standard dose vonoprazan therapy
Published in Scandinavian Journal of Gastroenterology, 2022
Satoshi Shinozaki, Hiroyuki Osawa, Yoshimasa Miura, Yoshikazu Hayashi, Hirotsugu Sakamoto, Tomonori Yano, Alan Kawarai Lefor, Hironori Yamamoto
A decreased number of parietal cells is considered to result in hypergastrinemia due to negative feedback from gastric G cells. Based on this mechanism, VPZ might be more effective in patients with severe atrophy compared to those with no atrophy. However, we previously reported that long-term VPZ therapy improved GERD and did not aggravate other abdominal symptoms regardless of the grade of gastric atrophy [11]. In the present study, it should be noted that there was an upper limit for serum gastrin levels with long-term VPZ therapy, which not accompanied by significant clinical symptoms. Since there are no reports demonstrating a definite causal relationship between serum gastrin level and symptoms, we believe that hypergastrinemia alone does not affect abdominal symptoms. This suggests that routine screening for serum gastrin levels is not recommended during acid suppression therapy. The acid suppression effect induced by VPZ is useful in long-term control of symptomatic GERD [11], PPI-resistant GERD [12] and severe reflux esophagitis [9]. Considering the risk-benefit balance together with the current data, an elevated gastrin level alone is not grounds to cease the long-term use of VPZ.
Clinical consequences of controversies in gastric physiology
Published in Scandinavian Journal of Gastroenterology, 2020
Taking into consideration that gastrin is a peptide hormone that accordingly has to interact with its membrane receptor to exert any effect, it is amazing that the interest on its role in tumorigeneses for a long-time was concentrated on the colon [62]. There is no known physiological gastrin receptor there, and more importantly, gastrin in vivo does not have any proliferative effect on this organ [63]. The sole cell with an undisputed stimulatory gastrin receptor is the ECL cell located in the oxyntic mucosa of the stomach. It is therefore strange that when a group examine the role of gastrin in gastric carcinogenesis, antral carcinomas were investigated [64]. Gastrin has no positive trophic effect on the antrum [63], and if there exists a gastrin receptor there, it would be expected to be a negative one located on the G cell.
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].