Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of regulatory peptides was studied in the separated epithelium, lamina propria, submucosa and muscularis externa of the human jejunum. Gastrin, secretin, gastric inhibitory polypeptide, enteroglucagon and neurotensin immunoreactivity were almost confined to the endocrine cell-containing mucosal epithelium (greater than 98% of the total content), only minor amounts of motilin being detected in non-epithelial layers (3.6 +/- 0.7%, mean +/- SEM, n = 7). Conversely, vasoactive intestinal polypeptide, substance P and mammalian bombesin were virtually limited to non-epithelial layers (greater than 99%). Only somatostatin was found in all layers (44 +/- 6.7% in the epithelium, 34 +/- 5.2% in the lamina propria, 13 +/- 2.9% in the submucosa, and 7.9 +/- 2.8% in the muscularis). Substance P was found in higher concentrations in the mucosa, compared to submucosa and muscle (56 +/- 10, 30 +/- 4.0 and 29 +/- 4.0 pmol/g, respectively), while vasoactive intestinal polypeptide was more abundant in the muscle (411 +/- 52 pmol/g) compared to mucosa and submucosa (228 +/- 64 and 219 +/- 31 pmol/g, respectively). Only low levels of mammalian bombesin were measured, mainly in the muscle (6.9 +/- 1.5 pmol/g, or 89 +/- 3.6% of total content).
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PMID:Regulatory peptide distribution in separated layers of the human jejunum. 360 2

Telenzepine is an analogue of pirenzepine with a higher potency and similar selectivity for M1-receptors in animals. In this placebo controlled, double blind, randomised study mean peptone stimulated gastric acid secretion (mean +/- SEM) of 10 male healthy subjects (58 +/- 6 mmol H+/3 h for placebo) was significantly and dose dependently inhibited by oral telenzepine (2 mg: 31 +/- 5, 3 mg: 23 +/- 5, 5 mg: 21 +/- 4 mmol H+/3 h). Telenzepine 3 and 5 mg were significantly stronger than pirenzepine 50 mg orally (37 +/- 8 mmol H+/3 h). Mean percentage acid inhibition was 37% for pirenzepine, and 48, 61, and 64% for 2, 3, and 5 mg telenzepine, respectively. Basal and peptone stimulated gastrin release was unaffected. Mean salivary output per three hours declined moderately from 156 +/- 45 g (placebo) to 136 +/- 45 g with pirenzepine and significantly to 88 +/- 28 g, 95 +/- 39 g and 39 +/- 13 g with telenzepine 2, 3, and 5 mg, respectively. There was a parallel effect on Na+, K+, Ca++ and amylase output in saliva. Near point vision was not altered by either drug. Pulse rates were lowered by both substances. Complaints of dry mouth were more frequent with telenzepine 5 mg. On a molar basis telenzepine proved to be a 25 and 50 times more potent inhibitor of gastric and salivary secretion, respectively.
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PMID:Telenzepine is at least 25 times more potent than pirenzepine--a dose response and comparative secretory study in man. 365 58

In 89 healthy full-term newborn infants, we studied the different contribution of gastrin 17 (G17) and gastrin 34 (G34) to neonatal hypergastrinemia and the G17 and G34 response to a meal in the first days of life. Serum concentrations of G17 and G34 were measured by radioimmunoassay specific for the NH2-terminus of G17 and G34 in 23 newborn infants in the cord blood and in 66 newborn infants before or 20 min after bottle-feeding. Basal serum G17 and G34 values were also obtained in 38 healthy fasting adults. Mean (+/- SEM) G17 levels in the cord blood were not different from those of the adult controls (29.28 +/- 4.16 versus 31.00 +/- 2.62 pg/ml) and increased significantly either at 12 h (48.06 +/- 7.32 pg/ml, p less than 0.025) or on the 4th day of life (80.56 +/- 9.99 pg/ml, p less than 0.01). Serum G34 levels in the cord blood were significantly higher than in adult controls (163.22 +/- 11.19 versus 126.68 +/- 5.57 pg/ml, p less than 0.005) and increased at 12 h of life (225.22 +/- 25.95 pg/ml, p less than 0.02), but no increase was found on the 4th day of life (204.87 +/- 18.08 pg/ml). Neither postprandial G17 nor G34 increases were found on the 1st or on the 4th day of postnatal life. The study supports the following conclusions: (a) neonatal hypergastrinemia is mainly due to G34 fraction; (b) the increased levels of gastrin on the 4th day of life are due to G17 fraction; (c) bottle-feeding does not stimulate either G17 or G34 release in the first 4 days of life.
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PMID:Gastrin 17 and gastrin 34, before and after a meal, in newborn infants. 369 65

The effects of synthetic [Asu1,7]-eel calcitonin (0.5 MRC unit/kg body weight intravenously for 30 min) on circulating levels of human calcitonin, calcium and gastrin were investigated in five patients with medullary carcinoma of the thyroid. Blood samples were obtained before and 15, 30, 60, 90, 120 and 180 min after commencement of infusion of [Asu1,7]-eel calcitonin. Plasma levels of human calcitonin were measured by radioimmunoassay. Cross-reactivity with [Asu1,7]-eel calcitonin in this assay was negligible. On infusion of [Asu1,7]-eel calcitonin, the mean plasma level of human calcitonin decreased significantly to 71.0 +/- 8.7% of the basal level (mean +/- SEM, P less than 0.05) after 30 min and 68.4 +/- 25.4% of the basal level (P less than 0.05) after 60 min. The serum calcium level also decreased significantly, but lagged behind the decrease of human calcitonin, being 95.1 +/- 0.7% of the basal level (P less than 0.01) at 120 min and 94.8 +/- 0.6% of the basal level (P less than 0.02) at 180 min. The mean plasma gastrin level did not change significantly on infusion of [Asu1,7]-eel calcitonin. In pooled data for all times, the percentage change in human calcitonin was not significantly correlated with either the percentage change in calcium (r = -0.25, P greater than 0.1) or the percentage change in gastrin (r = -0.38, P greater than 0.1).
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PMID:Eel calcitonin suppresses plasma human calcitonin levels in medullary carcinoma of the thyroid. 369 10

Our primary aim was to determine whether mucosal antrectomy decreases postcibal serum gastrin and gastric acid secretion. In four dogs with proximal gastric vagotomy and a Heidenhain pouch, mucosal antrectomy decreased the integrated postcibal serum gastrin response from a mean +/- SEM of 2.0 +/- 0.2 ng X h/mL before antrectomy to 0.8 +/- 0.1 ng X h/mL after antrectomy, while it decreased postcibal output of hydrochloric acid from the pouch from 9.5 +/- 3.3 mEq/7 h (9.5 +/- 3.3 mmol/7 h) to 4.3 +/- 2.2 mEq/7 h (4.3 +/- 2.2 mmol/7 h). However, these decreases were temporary in two of the four dogs. In five additional dogs without vagotomy, the distal, antral, mucosal gastrin level increased from 1 +/- 1 micrograms/g of tissue before mucosal antrectomy to 5 +/- 1 micrograms/g of tissue after the antrectomy. Moreover, gastrin and G cells were present in corporal mucosa transferred to the antrum in three of five dogs after the antrectomy, where none had been present in the corporal mucosa before the antrectomy. The conclusion was that mucosal antrectomy decreased serum gastrin and hydrochloric acid output from the stomach, but that these changes were counteracted in part by hyperplasia of residual G cells and G-cell neogenesis after the operation.
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PMID:Canine mucosal antrectomy. 371 17

The nude (athymic) mouse is currently used to study the effect of gastrin on cancer xenografts. We sought to develop a hypogastrinemia nude mouse model for use in evaluating the effect of hypogastrinemia on such xenografts. Thirty-six non-tumor-bearing nude mice were studied. Eighteen received a nutritionally complete liquid diet; eighteen received standard chow. Six mice from each group were weighed and killed (nonfasting) on days 2, 8, and 15. Mean serum gastrin levels (+/- SEM) for the control group were 118.7 +/- 7.5, 118.7 +/- 8.7, and 118.0 +/- 7.5 pg/ml on days 2, 8, and 15, respectively. Serum gastrin levels for the liquid diet group significantly decreased to 87.0 +/- 7.6, 88.0 +/- 9.7, and 66.7 +/- 9.6 pg/ml on the same days. Animals in both groups gained weight normally; there were no significant weight differences between the two groups at any point. No histological abnormalities were seen in stomach, small intestine, colon, cecum, liver, pancreas, spleen or kidney. However, the liquid diet group showed atrophic changes in colon: significant reductions in colon weight and RNA content on days 8 and 15, and significant reduction in colon protein content on day 8. This model of hypogastrinemia is reliable and inexpensive. The nonsurgical nature of the preparation allows excellent survival in this immunodeficient animal.
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PMID:Effect of liquid diet on nude mouse gastrointestinal tract. 372 91

Basal and food-stimulated levels of gastrin and pancreatic polypeptide (PP) were studied in 86 patients with non-ulcer dyspepsia (NUD), defined as chronic or recurrent epigastric pain without anatomical antecedents and without concomitant symptoms of irritable bowel. Thirteen patients with endoscopically confirmed duodenal ulcer disease (DU) and 13 healthy subjects constituted the reference groups. The mean basal gastrin concentration was moderately but significantly (p less than 0.05) higher in the NUD group than in the reference groups (24.3 +/- 1.6 (SEM) pmol/l in NUD, compared with 15.0 +/- 1.5 and 13.6 +/- 1.0 pmol/l among DU patients and healthy subjects, respectively). The well-established postprandial hypergastrinemia in duodenal ulcer patients could be confirmed in this study, and their gastrin response to food was significantly (p less than 0.01) greater than the responses observed both in healthy subjects and in NUD patients. The two latter groups did not differ significantly with regard to gastrin increments, but there was a tendency towards greater increases in the NUD group. A significantly (p less than 0.05) enhanced PP response to the test meal was observed among the DU patients, whereas the response pattern in NUD was closely similar to that in healthy subjects.
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PMID:Basal and food-stimulated levels of gastrin and pancreatic polypeptide in non-ulcer dyspepsia and duodenal ulcer. 372 53

Peptide YY (PYY) is a 36 amino acid peptide produced by mucosal endocrine cells of the ileum and colon which inhibits acid secretion and intestinal transit in man. To assess its effects on metabolites and digestive hormones PYY was infused into 18 fasting normal subjects at three dose levels (0.06, 0.19, and 0.57 pmol kg-1 min-1), each for a period of 1 h. During the infusions mean plasma PYY levels increased by 8, 25, and 73 pmol/liter, respectively. The mean disappearance half-time on stopping the infusions was 9.2 +/- 0.4 (SEM) min. The mean MCR was 7.3 +/- 0.7 ml kg-1 min-1 and the apparent volume of distribution was calculated to be 94 +/- 9 ml kg-1. During the highest dose infusion there was a significant increase in both systolic and diastolic blood pressure, of 8.6 +/- 3.7 mmHg (P less than 0.05) and 10.9 +/- 3.0 mmHg (P less than 0.01), respectively. PYY caused a significant 50% reduction in plasma pancreatic polypeptide concentrations (P less than 0.05) and a 55% reduction in circulating motilin levels (P less than 0.05). PYY had no significant effect on circulating concentrations of insulin, glucagon, gastrin, gastric inhibitory peptide, neurotensin, enteroglucagon, or vasoactive intestinal peptide. PYY also had no significant effect on circulating concentrations of glucose, lactate, glycerol, or nonesterified fatty acids. This recently discovered human intestinal hormonal peptide thus has significant effects both on gastrointestinal hormones (motilin and pancreatic polypeptide) and blood pressure in man, but appears not to influence glucose or lipid metabolism.
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PMID:Peptide YY kinetics and effects on blood pressure and circulating pancreatic and gastrointestinal hormones and metabolites in man. 375 28

This study was undertaken to determine whether histamine H2-receptors are involved in the regulation of gastrin secretion in man. Since previous studies on the effect of histamine H2-receptor blockade on gastrin release are conflicting, we have studied the effect of histamine infusion (130 nmol/kg/hr) with simultaneous H1-receptor blockade on gastrin release in healthy male subjects. Intragastric pH was maintained at 4.5 by continuous intragastric titration during all studies. Histamine did not affect gastrin release stimulated by infusion of bombesin (90 pmol/kg/hr) or by a peptone meal. Integrated gastrin secretion during bombesin plus histamine was 767 +/- 151 pmol X min/liter (+/- SEM), compared to 757 +/- 144 pmol X min/liter during bombesin plus saline (not significant), whereas integrated meal-stimulated gastrin release was 1666 +/- 456 pmol X min/liter during histamine and 1856 +/- 492 pmol X min/liter during saline. It is concluded that histamine H2-receptors do not seem to be involved in the regulation of gastrin secretion in man.
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PMID:Effect of histamine H2-receptor stimulation on bombesin- and peptone-stimulated gastrin release in man. 375 24

Duodenal gastrin concentration was measured in endoscopic forceps biopsy specimens of the juxta-pyloric duodenal mucosa in patients with various gastrointestinal disorders. Duodenal gastrin concentration was 5.9 +/- 1.2 ng/mg (mean +/- 1 SEM) in control patients. Duodenal gastrin concentration was similar to control values in patients with duodenal ulcer, pyloric channel ulcer, vagotomy and pyloroplasty, and gastric atrophy and hypergastrinemia. In gastric ulcer patients, duodenal gastrin concentration, 2.8 +/- 0.6 ng/mg, was significantly less than the control value (P less than 0.05). Duodenal gastrin concentration was approximately one third of antral gastrin concentration in control, duodenal ulcer, and gastric ulcer patients and was approximately one fifth of antral gastrin concentration in vagotomy and pyloroplasty patients and gastric atrophy patients. Duodenal and antral gastrin concentrations were significantly correlated in normal controls and in gastric ulcer patients. The finding of normal duodenal gastrin concentration in patients with vagotomy and pyloroplasty and patients with gastric atrophy suggests that, unlike antral gastrin concentration, duodenal gastrin concentration is unaffected by a decrease in acid secretion rate. The low duodenal gastrin concentration in gastric ulcer patients indicates that the duodenum may be involved in the pathophysiology of gastric ulcer disease.
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PMID:Duodenal gastrin concentration in upper gastrointestinal disorders. 376 3


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