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)

Unspecific binding of immunoglobulins to gastrin, somatostain and glucagon cells of the gastrointestinal mucosa or pancreas has been found to occur through a nonantigen-antibody mechanism mediated by the C14 fraction of complement. The phenomenon represents an important drawback in hormone immunohistochemistry, which can be overcome by using complement deprived, highly dilute anti-hormone sera.
J Histochem Cytochem 1979 Sep
PMID:Complement-mediated binding of immunoglobulins to some endocrine cells of the pancreas and gut. 47 71

Immunocytochemical studies habe shown that many peptides which profoundly affect the endocrine and exocrine functions of the pancreas are localized to neurons. In the cat, such peptidergic nerves appear to innervate ganglia, islets and blood vessels of the pancreas, whereas their contributions to exocrine cells are minor. Our studies suggest that pancreatic ganglia represent one major site of action of the peptides and that, in addition, nerves containing the vasoactive intestinal polypeptide and gastrin/CCK-related peptides profoundly affect pancreatic blood flow and insulin secretion, respectively.
J Histochem Cytochem 1979 Sep
PMID:Innervation of the pancreas by substance P, enkephalin, vasoactive intestinal polypeptide and gastrin/CCK immunoractive nerves. 47 72

This study tested the hypothesis that the inhibitory action of secretin on gastrin-stimulated gastric acid and pepsin secretion is comprised in animals harboring intestinal stages of the parasite Trichinella spiralis. Pentagastrin-stimulated acid and pepsin secretion, and the influence of secretin on these processes, were measured in dogs prepared with gastric fistulas and Heidenhain pouches. Dogs were studied before and after infection with 10(4) T. spiralis larvae/kg body weight. Gastric secretion was stimulated by constant intravenous infusion of pentagastrin, 1 microgram/kg per hour. Exogenous secretin inhibited pentagastrin-stimulated acid and pepsin output from both the main stomach and Heidenhain pouch in infected as well as in the uninfected dogs. Identical inhibition was observed in uninfected dogs during duodenal infusion with HCl to release endogenous secretin. In contrast, duodenal stimulation with HCl did not inhibit acid and pepsin secretion in dogs tested during the 1st week following infection. Results support the conclusion that the regulatory effect of secretin on gastrin-stimulated gastric secretion is impaired during the early phase of infection, and is due to depressed synthesis or release of secretin from duodenal mucosa.
Am J Trop Med Hyg 1979 Sep
PMID:Influence of parasitism on secretin-inhibited gastric secretion. 48 66

An intravenous bolus of pentagastrin significantly increased the amplitude and duration of oesophageal body contractions in seven patients with diffuse oesophageal spasm (DES) when compared with five normal subjects (P greater than 0.05). In order to determine whether this stimulation also occurred at physiological gastrin concentrations, the effect of an intravenous infusion of gastrin heptadecapeptide (G17), 25 pmol/kg-h, on oesophageal contractions was studied in DES patients. G17 had no significant effect on the amplitude and duration of oesophageal contractions compared with a saline control. This dose of G17 was near the D50 for gastric acid secretion and produced a rise in serum gastrin concentration comparable with a meal. G17 infusions at doses of 100 and 200 pmol/kg-h increased the amplitude and duration of oesophageal contractions, but the corresponding serum gastrin concentrations were higher than postprandial levels. Thus, endogenous fluctuations in serum gastrin heptadecapeptide, alone, are unlikely to alter oesophageal contractions in DES patients.
Gut 1979 Sep
PMID:Effect of gastrin heptadecapeptide (G17) on oesophageal contractions in patients with diffuse oesophageal spasm. 49 13

Basal circulating levels of gastrin, somatostatin, and pancreatic polypeptide were measured in 30 chronic haemodialysis patients. Five patients had considerably raised serum gastrin (greater than 400 pmol/1) and also gastric achlorhydria while 75% of the patients who had normal (less than 55 pmol/1) or moderately increased (less than 400 pmol/1) serum gastrin had raised maximal acid outputs. Patients with serum gastrin greater than 400 pmol/1 had significantly lower plasma concentrations of somatostatin compared with both healthy individuals and uaremic patients with normal gastrin levels. Raised serum concentrations of pancreatic polypeptide were observed in the majority of the patients but no correlation was found between this peptide and gastric acid secretion or circulating levels of gastrin and somatostatin, respectively. Prolonged circulation time for gastrin and pancreatic polypeptide was demonstrated after food stimulation. Prolonged gastrin stimulation of the parietal cell mass may lead to work hypertrophy and gastric acid hypersecretion. Whether long-standing over-stimulation by gastrin also may induce atrophy of the cells remains to be studied.
Gut 1979 Sep
PMID:Gastric acid secretion in uraemia and circulating levels of gastrin, somatostatin, and pancreatic polypeptide. 49 15

131 patients operated on for gastric ulcer according to Gillroth II were investigated with gastroscopy and biopsy. The histology of the gastric mucosa was correlated with the time elapsed since resection. In most cases gastritis shows no difference between anastomosis and stump. In up to 12% gastritis in the stump was more pronounced that at the anastomosis. In the stump any form of gastritis can be seen even more than 20 years afer resection. Atrophic changes are more often to be found in the resected stomach and develop more rapidly than in the normal stomach. They probably result from the coincidence of the lost protective function of the mucous membrane after resection of the gastrin-producing antrum with the potentially damaging action of the contents of small intestine.
Z Gastroenterol 1979 Sep
PMID:[The histology of gastric mucosa in B II-stomach (author's transl)]. 50 60

The existence of a stimulatory intestinal phase of gastric acid secretion has been suspected, but largely ignored, for many years. Recently, however, it has become clear that the intestinal phase plays an important role in acid production during digestion. The intestinal phase is of additional interest in relation to the profound gastric acid hypersecretion associated with portacaval shunt (PCS). Substantial evidence indicates that PCS-related gastric hypersecretion is due to unmasking of the intestinal phase by hepatic bypass of a humoral stimulant in portal blood that is normally degraded to a considerable extent by the liver. Studies in our laboratory during the past 12 years have provided strong physiologic evidence for humoral mediation of both the intestinal phase of gastric secretion and of PCS-related hypersecretion by a hormone that arises in the small intestine, particularly in the jejunum. Furthermore, our studies have demonstrated that this intestinal phase hormone (IPH) exists in humans as well as in dogs, rats, and pigs. Additionally, recent work by a number of investigators, as well as by our group, has provided convincing evidence that IPH is different from any of the known gastric stimulatory hormones. With these physiologic observations as a background, we have used a classical method for extracting acidic peptides to prepare a hog intestinal mucosa extract (HIME) that has all of the known physiologic properties of an IPH. Specifically, HIME contains a potent stimulant of gastric acid secretion that acts according to a linear dose-response relationship; that is not gastrin in any of its immunoassayable forms; that significantly augments the maximal acid secretory responses to pentagastrin, gastrin, CCK, and histamine; and that is substantially degraded by the liver, in contrast to gastrin and CCK. Efforts at isolating the gastric stimulatory substance in HIME suggest that it is a peptide of low molecular weight. Work directed at isolating IPH in pure form and identifying it is in progress.
World J Surg 1979 Sep 20
PMID:The intestinal phase hormone. 51 73

Several gastrointestinal peptides with proven or suggested endocrine or paracrine functions influence gastric acid secretion, gastrointestinal motility, and mucosal blood flow. Increased or decreased release of such factors could participate in the pathogenesis of duodenal ulcer disease by inducing increased gastric acid concentration in the duodenal bulb. To date, increased stimulation of parietal cells by gastrin has been demonstrated only in patients with gastrinoma, G-cell hyperplasia, gastric outlet obstruction, hyperparathyroidism, excluded antrum, and short bowel syndrome, but not in the usual duodenal ulcer disease. Also, a defective inhibition of parietal cell function by endocrine or paracrine factors, such as gastric inhibitory polypeptide, secretin, somatostatin and vasoactive intestinal polypeptide, seems not to exist in patients with duodenal ulcer disease. However, as long as the physiology of gastrointestinal peptides in gastric secretion and motility is not understood, a possible role of these factors in the pathogenesis of simple duodenal ulcer disease cannot be excluded.
World J Surg 1979 Sep 20
PMID:Endocrinology of duodenal ulcer. 51 78

The effect of gastrin on DNA synthesis and mitotic activity in the mucosa of the upper-gastrointestinal tract was explored in unanesthetized rats with a gastric fistula. Animals were killed at 4-hr intervals, after starting a 3-hr intravenous infusion with the lowest dose of gastrin provoking a maximal acid output. Tritiated thymidine was injected 1 hr before killing. Autoradiography was used, and labeling and mitotic indices were estimated in the fundic, antral, duodenal, and jejunal mucosa. The proliferative activity in the fundic, duodenal, and jejunal glands was significantly increased 16 hr after the administration of gastrin. In the antral glands, however, a significant decrease in both labeling and mitotic indices was observed. Rhythmic variations in proliferative activity were observed in the antral, duodenal, and jejunal mucosa in control animals. They were different from those in the gastrin-treated animals. Our data confirm the trophic action of gastrin in the fundic, duodenal, and jejunal mucosa. They also indicate an inhibitory effect of this hormone on cell proliferation in the antral mucosa.
Am J Dig Dis 1977 Sep
PMID:Opposite effects of gastrin on cell proliferation in the antrum and other parts of the upper-gastrointestinal tract in the rat. 56 37

Eight infants with cow's milk intolerance (CMI) were studied for basal and maximal gastric acid secretion and the fasting serum gastrin level. All these patients had clinical malabsorption. Jejunal biopsies revealed subtotal villous atrophy in six children and slight changes in the remaining two. The mean maximal acid secretion in the infants with CMI was significantly decreased being 85 +/- 78 mumol/h/kg (mean +/- SD), as compared with a control group of the same age with a corresponding value of 233 +/- 66 mumol/h/kg. The fasting serum gastrin level was elevated, being 104 +/- 116 pmol/l in the study group and 37 +/- 10 in the controls. Three infants with CMI underwent gastric biopsy. Marked changes with epithelial degeneration and prominent cellularity in the lamina propria were seen in two patients. The injury was most severe in the antrum of the stomach. When these patients with CMI were treated with human or soy milk, the maximal acid secretion returned normal in six months.
Eur J Pediatr 1979 Sep
PMID:Impaired gastric function in children with cow's milk intolerance. 57 86


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