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)

Serum gastrin concentration was measured in six male subjects before and after a beef meal, with and without 100 g of oral glucose being given 30 min previously. There was a pronounced inhibition of beef-stimulated gastrin secretion after the oral glucose load.
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PMID:Inhibition of meal-stimulated gastrin secretion after oral glucose. 95 55

Intravenous infusion of isoproterenol, a beta-adrenergic receptor stimulatory agent, increased serum gastrin concentration significantly more in patients with a duodenal ulcer than in healthy subjects. The rise in pulse rate, blood glucose concentration and in serum insulin was the same in both groups of subjects. Gastrin secretion was also increased significantly more in the patients than in the control subjects after a beef-meal. Basal serum gastrin concentrations were higher in the patients than in the control subjects and correlated to the rise in serum gastrin during both tests in the patients with a duodenal ulcer. Isoproterenol and meal stimulated gastrin secretion, expressed as percent of the basal value, were twice as higher in the patients as in the control subjects. The combined administration of isoproterenol and the meal had an additive effect on the rise in serum gastrin. Isoproterenol stimulated gastrin secretion was completely suppressed by propranolol, a beta-adrenergic receptor blocking agent, which had no effect on meal stimulated gastrin secretion. It is concluded that the mechanism of the hypersecretion of gastrin in patients with a duodenal ulcer did not involve a specific abnormality of the beta-adrenergic receptor or the receptor which recognized proteins and their digested products. There is no established role of beta-adrenergic receptor activity in the hypersecretion of gastrin in patients with duodenal ulcers. It is suggested that the beta-adrenergic receptor may have some yet unknown function unrelated to the acute secretory response of gastrin.
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PMID:The role of the beta-adrnergic receptor in the secretion of gastrin: studies in normal subjects and in patients with duodenal ulcers. 97 1

The effect of graded doses (0.125, 0.500, 1.00 and 2.00 mug per kg per hr) of intravenous synthetic human gastrin I (SHG) on jejunal transport of water, electrolytes, and glucose from a glucose-saline solution (solution II) was studied in 12 healthy volunteers, using an intestinal perfusion technique with a proximal occluding balloon. SHG when infused at rates of 0.500 mug per kg per hr or greater significantly reduced water and electrolyte absorption; this effect was linearly related to the dose and reached 40 to 60% of basal absorption (and only 10% for glucose) with the highest dose; insorption of sodium and water were significantly decreased by SHG. In a further group of 9 subjects no effect of SHG (2 mug per kg per hr) was found on jejunal absorption from a mannitol-saline solution (solution I) and on ileal absorption from solutions I and II; in 5 additional subjects, SHG did not decrease jejunal transit time of intraluminal fluid. There was no increase in serum thyrocalcitonin during SHG infusion. It is proposed that SHG selectively depresses the glucose-stimulated sodium transport as suggested by the reduction of the rate of net sodium absorption per micromole of glucose absorbed during SHG infusion. Physiological and pathological implications of these findings are discussed, especially in the light of the circulating levels of immunoreactive gastrin achieved during SHG infusion.
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PMID:Effects of synthetic human gastrin I on movements on water, electrolytes, and glucose across the human small intestine. 99 81

Glucose-stimulated insulin secretion was measured in six normal subjects in the resting supine position, during standing, and during a period of moderate exercise in the supine position. Plasma noradrenaline averaged 0.26 ng/ml in the supine, resting position and rose to 0.57 and 0.61 ng/ml at the end of the standing experiment and the exercise period, respectively. Plasma adrenaline was unchanged in the standing position but rose threefold during exercise (to 0.09 ng/ml). Serum gastrin tended to decrease in all three experiments after the injection of glucose. Glucose-stimulated insulin secretion was the same during the first 10 min after the injection of glucose in the three experiments. It is concluded that a moderate increase in adrenergic activity has no influence on glucose-stimulated insulin secretion.
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PMID:The effect of standing and exercise on plasma catecholamines, serum insulin, and serum gastrin. 100 47

The insulin response to oral glucose ingestion was measured in six patients with the Zollinger-Ellison (ZE) syndrome, five patients with partial gastrectomy (antrectomy for duodenal ulcer) and six matched normal subjects. The blood glucose curves were similar in ZE-patients and gastrectomized controls and significantly above the glucose concentrations in normal controls. The insulin response was three-doubled in ZE-patients, whereas gastrectomized controls only doubled their response in comparison with the normal subjects. Treatment of a hepatic gastrinoma by streptozotocin infusion into the hepatic artery in a patient with diabetes mellitus and hyperinsulinism almost normalized his glucose tolerance and insulin secretion. The results demonstrate that the ZE-syndrome is associated with increased insulin release. We suggest that the hyperinsulinism partly is a consequence of previous gastric surgery and partly due to the insulinogenic effect of gastrin.
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PMID:Insulin secretion in the Zollinger-Ellison syndrome. 106 42

The effect of glucagon on gastric acid and pepsin secretion, basal or stimulated by a meal, pentagastrin and histamine, was studied in duodenal ulcer patients. Intravenous glucagon infused in graded doses ranging from 6.2 to 50 mug per kg-hr produced a dose-related inhibition of pentagastrin-induced acid secretion reaching about 40% of the control level at the dose of 50 mug per kg-hr. Acid inhibition was paralleled by a decrease in the pepsin output and serum calcium level and was accompanied by a rise in the blood glucose concentration. Glucagon used in a standard dose of 25 mug per kg-hr produced about 50% inhibition of acid secretion induced by a meal (measured by intragastric titration) accompanied by a significant decrease in the serum gastrin level measured by radioimmunoassay. Histamine-induced secretion was only slightly inhibited by glucagon, and the degree of inhibition for acid (25%) and pepsin (20%) secretion was statistically insignificant.
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PMID:Effect of glucagon on meal-induced gastric secretion in man. 108 77

In various nutrient-limited cultures of either Escherichia coli W4597(K) or G34 a 10-fold range of rates of glycogen synthesis is observed while the energy charge values (0.86 plus or minus 0.01) and glucose 6-phosphate levels are essentially the same in each condition. The steady state level of fructose 1,6-diphosphate in these cultures varies from experiment to experiment as a function of the observed rate of glycogen synthesis. These data were fitted to the Hill equation by a nonlinear regression analysis and the statistically most probable values obtained for the Hill coefficient (n), A0.5, and V were, respectively, 2.08, 0.82mM, and 1030 mumol/g of protein per hour. The values of the first two parameters agree well with values available at energy charge 0.85 for the in vitro synthesis of ADPG by the ADPG synthetase of E. coli. When the difference in the glucose 1-phosphate concentration used in the studies in vitro from the apparent glucose 1-phosphate concentration in vivo (estimated from the glucose 6-phosphate levels) is considered, the in vitro value of V (1140 mumol of ADPG synthesized per g of protein per hour) is quite similar to the value of V (1030 mumol of glucose incorporated into glycogen per g of protein per hour) for glycogen synthesis in vivo. The close agreement of the values of the parameters of the Hill equation for glycogen synthesis in vivo to the values obtained for ADPG synthesis in vitro provides the most quantitative evidence yet obtained that allosteric regulation of bacterial glycogen synthesis functions in vivo.
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PMID:Evidence for the allosteric regulation of glycogen synthesis in the intact Escherichia coli cell. Agreement of the values of the parameters of the Hill equation fitted to data for glycogen synthesis in vivo with the abailable values obtained in vitro with adenosine diphosphoglucose synthetase. 109 Jun 18

In cultures of Escherichia coli W4597(K) and G34 under various nutritional conditions the rates of glucose utilization and cellular levels of fructose-1,6-P2 are quantitatively related by the Hill equation where the value of the Hill coefficient is approximately equal to 2. This is the first evidence that fructose-P2, or any metabolite which covaries with fructose-P2, modulates glucose utilization in E. coli. In light of previous observations from our laboratory this new observation and those in the succeeding report provide the first evidence that in E. coli glycolysis, glycogen synthesis and glucose utilization are coordinately regulated, thus providing for the coupling of ATP utilization and production under various metabolic circumstances. Alterations in the level of ATP apparently affect the velocity of phosphofructokinase, the rate-limiting enzyme in glycolysis, altering the cellular levels of glucose-6-P or fructose-P2. Changes in the levels of these hexose phosphates are quantitatively related to alterations in the rates of glucose utilization and glycogen synthesis in the intact E. coli cell.
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PMID:Evidence for the coordinate control of glycogen synthesis, glucose utilization, and glycolysis in Escherichia coli. I. Quantitative covariance of the rate of glucose utilization and the cellular level of fructose 1,6-diphosphate during exponential growth and nutrient limitation. 110 Jun 22

In cultures of Escherichia coli W4597(K) and G34 under various nutritional conditions the rates of glucose utilization and cellular levels of fructose-1,6-P2 are quantitatively related by the Hill equation where the value of the Hill coefficient is approximately equal to 2. This is the first evidence that fructose-P2, or any metabolite which covaries with fructose-P2, modulates glucose utilization in E. coli. In light of previous observations from our laboratory this new observation and those in the succeeding report provide the first evidence that in E. coli glycolsis, glycogen synthesis and glucose utilization are coordinately regulated, thus providing for the coupling of ATP utilization and production under various metabolic circumstances. Alterations in the level of ATP apparently affect the velocity of phosphofructokinase, the rate-limiting enzyme in glycolsis, altering the cellular levels of glucose-6-P or fructose-P2. Changes in the levels of these hexose phosphates are quantitatively related to alterations in the rates of glucose utilization and glycogen synthesis in the intact E. coli cell.
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PMID:Evidence for the coordinate control of glycogen synthesis, glucose utilization, and glycolysis in Escherichia coli. II. Quantitative correlation of the inhibition of glycogen synthesis and the stimulation of glucose utilization by 2,4-dinitrophenol with the effects on the cellular levels of glucose 6-phosphate, fructose, 1,6-diphosphate, and total adenylates. 110 Jun 23

Pancreatico-duodenectomy was performed in 11 patients for malignant or inflammatory tumours of the head of the pancreas or the region of the papilla. Digestive and endocrine functions were determined after the operation. In all cases faecal fat values were abnormal, indicating a 90% loss of pancreas. 14C-exhalation measurement, chymotrypsin determination in stool, and amylose tolerance test were also performed. Oral glucose-tolerance tests with plasma-insulin measurement indicated asymptomatic diabetes mellitus in the majority of patients. Two patients whose diabetes was controlled by tablets before the operation required insulin treatment afterwards. A decreased serum-gastrin level proved the existence of gastric and extragastric sources of gastrin.
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PMID:[Digestive and endocrine functions after partial duodeno-pancreatectomy]. 111 29


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