Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Quantitative electron microscopical measurements performed on gastric zymogen cells were aimed at determinations of size and volume density of the zymogen granules, and size of cell and nuclear profiles. 17 groups of rats each comprising 6-8 animals were investigated: five of these groups were used to study the influence of fasting and feeding, three groups were killed at different intervals after a pilocarpine injection, and four other groups were investigated after an atropine injection. The remaining five groups of rats were operated on: vagotomy was performed on one group, vagotomy + pyloroplasty on another, pyloroplasty on the third group, and antrectomy on the last two groups. The operated rats were sacrificed 4 or 10 weeks after the operations. Pilocarpine was more effective than feeding in reducing the size and the amount of zymogen granules. After atropine the size and amount of zymogen granules tended to increase. Ten weeks after pyloroplasty, vagotomy + pyloroplasty, or antrectomy the mean size of the zymogen cells was reduced. Loss of trophic vagal impulses, duodenal regurgitation, and abnormal serum gastrin levels are factors which might be responsible for the zymogen cell hypotrophy in operated rats.
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PMID:Quantitative ultrastructural studies on rat gastric zymogen cells under different physiological and experimental conditions. 65 45

Vagally innervated antral pouches were created in adult mongrel dogs, the interiors of these antral pouches were perfused with glycocholate, taurocholate, canine bile and human pancreatic juice, and antral function was investigated from the viewpoint of gastric endocrine and exocrine response. Perfusion with glycocholate and taurocholate of 20 mM induced a significant increase in gastric acid secretion as well as serum gastrin secretory response. Perfusion with canine bile and human pancreatic juice induced a pronounced increase in serum gastrin levels as well as gastric acid secretion starting immediately after the beginning of perfusion, and serum gastrin secretory response also displayed a marked increase. These results demonstrated that the regurgitation into the stomach of duodenal fluid containing bile and pancreatic juice, constitutes one factor causing increased serum gastrin levels and gastric acid secretion.
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PMID:[An experimental study of the effect of perfusion of duodenal juices in the vagally innervated antral pouch upon gastric endocrine and exocrine function]. 225 Mar 75

The Willmen gastric bubble has been used as an adjunct to weight loss in morbidly obese patients. 35 patients with morbid obesity were studied with routine manometry, esophageal 24-h-pH-measurement, and gastric emptying studies before and 4 weeks after bubble placement. During emptying studies blood samples were taken to measure gastrin, PP, CCK, VIP, neurotensin and insulin. No patient developed heartburn or regurgitation after bubble placement. Esophageal motility and LES function remained unchanged. There was no important pathological gastroesophageal reflux before and after gastric bubble. The gastric emptying time of solid food was unchanged by gastric bubble placement and the emptying time of liquids was accelerated up to normal. In patients with fasting gastrin levels less than 20 pg/ml at the beginning of the first test we found no differences in gastrin release before and after bubble insertion. In patients with primary high fasting values gastrin release was significantly increased. CCK, VIP, neurotensin and insulin levels were unchanged. With PP we measured significantly raised fasting levels after gastric bubble. We conclude that esophageal and LES functions are not altered by Willmen gastric bubble placement and that primary retardation of fluids is changed to normal. Bubble induced gastric tension increases fasting PP. In case of high fasting gastrin the bubble leads to an extremely high food response without any clinical signs.
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PMID:[Does the stomach balloon modify the function of the esophagus and lower esophageal sphincter, stomach emptying and release of gastrointestinal peptides?]. 266 61

We have established an experimental model of chronic gastric ulcer, in rats which transection of the lower horizontal portion of the duodenum and anastomosis of the forestomach to the upper part of the jejunum caused regurgitation of all duodenal juice into the stomach. After 3, 6, 12, and 30 wk, all treated rats developed an ulcer in the prepyloric region on the lesser curvature of the stomach. More than half of the antrum was finally involved in the ulcer. Histologic studies revealed chronic ulcers quite similar to human ones. As a control series, transection at the pylorus failed to produce an ulcer. Although many papers have appeared regarding the experimental production of chronic gastric ulcer, most of the studies reported have applied chemicals, drugs, or mechanical injury to the gastric mucosa. Our model produced chronic regurgitation of duodenal juice as a natural phenomenon, and uniformly resulted in ulcer formation. Intragastric total bile acid concentrations were significantly elevated in the reflux group. Serum gastrin levels, the thickness of the fundic mucosa, and the height of fundic gland were also significantly increased. Thus, the detergent action of bile acids and the increased acid secretion were assumed to play an important role in ulcer formation. Further studies using this model are warranted on the pathogenesis of chronic peptic ulceration.
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PMID:A new model for production of chronic gastric ulcer by duodenogastric reflux in rats. 356 68

It has been thought that upper intestinal symptoms of heartburn, regurgitation, belching, and chest pain experienced during exercise may represent esophageal dysfunction. The aim of this study is to examine esophageal function during moderate exercise in asymptomatic healthy athletes. Six healthy male athletes were exercised for 2 h on a treadmill set at a workload of 50% of their maximum oxygen uptake. Esophageal motility studies were performed immediately before, immediately after, and 1 h after the exercise. The mean lower esophageal sphincter pressure increased from a base line of 24 to 32 mm Hg immediately postexercise (p less than .01), reducing to 27 mm Hg after 1 hour rest. The mean amplitude and duration of esophageal peristalsis remained unchanged throughout the study. The significance of the lower esophageal sphincter pressure increase with moderate exercise is unknown but may relate to the observed exercise-induced increase in serum motilin, gastrin, and catecholamines.
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PMID:Effect of moderate exercise on esophageal function in asymptomatic athletes. 377 51

A 46-year-old Chinese woman was admitted to our hospital because of presence of space-occupying lesions in the liver for 2 months in April, 2015. She had a family history of multiple endocrine neoplasia type 1 (MEN1) and physical examination is unremarkable. Previously, she has performed surgery for primary pituitary tumor in 2002 and radiosurgery for its recurrence. Around December 2014, she suffered from abdominal discomfort associated with regurgitation and gastroscopy revealed "gastroduodenal ulcers", along with elevated gastrin. Next, both magnetic resonance and computed tomography imaging showed multiple intrahepatic lesions, the PET-CT unveiled uptake pattern of 18F-FDG in duodenum and multiple intrahepatic lesions, resembling the appearance of metastatic gastrinoma. The octreotide scan gave identical results. The parathyroid SPECT scans showed abnormal concentrations of radioactivity in right parathyroid. She also had an elevated serum chromogranin A (CgA) level. There was medical evidence to show that she is metastatic MEN1. Although multiple liver metastases, they were considered to be resectable after MDT consultation. The intraoperative exploration found a 1.5 cm tumor on the surface of the tail of the pancreas, a 12 cm retroperitoneal lipoma and two liver metastases, sized 3.5 cm and 1.5 cm, respectively. All these tumors were completely removed. For pancreatic tumor, pathological findings met the diagnostic criteria of neuroendocrine tumor (NET) (G2). Immunohistochemistry revealed neuroendocrine areas were diffusely positive for ATRX, DAXX, SSR2, SSR5 and CgA. For lipoma, the FISH results were negative for CDK4 and MDM2 genes. Postoperatively, adjuvant therapy with octreotide was applied. This case suggested that, as for metastatic gastrinoma, a potentially curative surgical debulking should be considered when a resection of complete or more than 90% of metastatic lesions along with the primary site could be achieved, which is helpful to control symptoms and delay the subsequent need for therapy.
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PMID:Metastatic multiple endocrine neoplasia type 1: report of one case. 2813 39