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)

The insulin and gastrin response to oral glucose, intravenous glucose, or a protein-rich meal were measured in 44 nondiabetic patients with pernicious anemia (PA) and in 44 control subjects. 36 of the PA-patients had hypergastrinemia, while serum gastrin concentrations in the remaining eight patients were below normal. Three hypergastrinemic PA-patients were in addition studied during an oral glucose loading with synchronous intravenous infusion of gastrin-17. During both oral and intravenous glucose tests blood glucose concentrations were similar in patients and in controls. After ingestion of protein blood glucose concentrations in PA-patients with hypergastrinemia were above those of the controls (P less than 0.05). Parenteral infusion of gastrin-17 during oral glucose loading also increased blood glucose concentrations above the levels observed after glucose alone. In PA-patients with hypergastrinemia the insulin response was augmented in all tests. In patients with hypogastrinemia serum insulin concentrations were lower than normal in the fasting state and during stimulation with glucose intravenously (P less than 0.01). In hypergastrinemic patients serum gastrin concentrations decreased after oral as well as intravenous glucose administration. The decrease was larger during the oral test. In hypogastrinemia oral glucose induced, as in controls, a small initial rise followed by a slow fall in serum gastrin concentrations. No variations were seen in these patients during the intravenous glucose infusion. Gel filtration of serum from hypergastrinemic patients disclosed a decrease in the concentrations of all four main components of gastrin during the glucose loadings. Taken together with earlier studies on the effect of exogenous gastrin the results suggest that endogenous hypergastrinemia induces hyperglycemia and potentiates insulin secretion. In contrast hypogastrinemia is associated with hypoinsulinism.
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PMID:Disturbed islet-cell function related to endogenous gastrin release. Studies on insulin secretion and glucose tolerance in pernicious anemia. 77 30

This study examines the effect of prolonged absence of oral food intake on structural parameters of the gastrointestinal tract in rats maintained nutritionally by intravenous feeding for up to 3 weeks. During this time, their body weights increased by 22%. Controls fed a nearly isocaloric oral diet were sham operated and harnessed in the same manner as their parenterally fed counterparts. Parenteral feeding resulted in a significant decrease in the weights (per 100 g body weight) of the oxyntic gland area of the stomach, small intestine, and pancreas. The weights of the spleen, testes, kidneys, and antral region of the stomach were unaltered. In the small intestine there was a significant loss of DNA and a near doubling of the RNA:DNA ratio in the parenterally fed animals. In the absence of an oral diet antral gastrin levels decreased to one-thirtieth of the control level. The following conclusions are suggested by these results. First, the oral intake and/or physical presence of food within the gastrointestinal tract are necessary for structural maintenance of some tissues of that tract. Second, the disproportionate decrease in weight that occurs in certain tissues is apparently unrelated to the absence of nutrients which might normally be utilized directly from the lumen. Third, maintenance of normal tissue stores of the hormone, gastrin, is dependent on stimuli provided by oral ingestion and the presence of food in the gastrointestinal tract.
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PMID:Structural and hormonal alterations in the gastrointestinal tract of parenterally fed rats. 80 78

The effect of continuous intraduodenal enteral nutrition on gastric pH was compared with the effects of fasting and of parenteral and standard nutrition control regimens containing equal amounts of carbohydrate, protein, and lipid. Eleven healthy volunteers underwent four 24-hour intragastric pH-metry studies; serum glucose, calcium, immunoreactive insulin and gastrin levels were determined during fasting and enteral and parenteral regimens. Median 24-hour gastric pH during enteral nutrition (group median pH 1.4) was lower than during parenteral nutrition (pH 1.9; P = 0.0039 vs. enteral) but was not different from fasting (pH 1.4) or standard nutrition (pH 1.6) values. Median 24-hour serum glucose levels during enteral nutrition (group median, 4.8 mmol/L) were higher than during fasting (4.0 mmol/L; P = 0.00098 vs. enteral) and lower than during parenteral nutrition (5.3 mmol/L; P = 0.0039 vs. enteral). Median 24-hour serum insulin levels during enteral nutrition (group median, 22.9 mU/L) were higher than during fasting (group median, 9.2 mU/L; P = 0.00098 vs. enteral) but similar to levels during parenteral nutrition (23.3 mU/L). Neither median 24-hour gastrin levels nor calcium levels were affected by any nutrition regimen. Thus, continuous enteral nutrition produces gastric pH values similar to those seen with fasting or standard nutrition, suggesting that, under most physiological conditions, gastric acidity is subject to close feedback control. Parenteral nutrition increases gastric pH, suggesting that systemic nutrients may influence this feedback mechanism.
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PMID:The effect of continuous enteral nutrition on gastric acidity in humans. 156 60

Parenteral nutrition has been advocated for and used in clinical situations in which provision of calories without stimulation of pancreatic secretion is desired. A recent report, however, provided evidence for substantial stimulation of pancreatic secretion after parenteral administration of amino acids and fat. We have studied the effect of intravenous administration of crystalline amino acids and lipid on pancreatic protein secretion and release of gastrointestinal hormones in five dogs with chronic pancreatic fistulas. The amino acids were given as a 4.25% solution in 5% glucose at 2 gm/hr. Parenteral fat was administered as Intralipid 10% at 3.5 ml/kg/hr. Plasma concentrations of cholecystokinin (CCK) and pancreatic polypeptide (PP) and serum concentrations of gastrin, measured by radioimmunoassay, were determined before, and at intervals during, infusion of amino acids and fat. Pancreatic juice was collected simultaneously with blood sampling, and volume and protein output were measured. Basal concentrations of CCK, PP, and gastrin were not affected by intravenous infusion of amino acids. Pancreatic protein secretion and volume were also unaffected by parenteral amino acids. Parenteral infusion of fat resulted in a significant inhibition of integrated gastrin release but had no effect on plasma concentrations or integrated release of CCK or PP. Neither the volume nor protein output of pancreatic secretion was affected by intravenous fat administration. In summary, no stimulation of pancreatic secretion or release of CCK, PP, or gastrin occurred as a result of parenteral amino acid or fat administration. There is, therefore, no contraindication to the use of parenteral nutrition in situations in which it is desirable to keep the pancreas at rest.
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PMID:Pancreatic protein secretion and gastrointestinal hormone release in response to parenteral amino acids and lipid in dogs. 681 82

The effects of cyclic adenosine monophosphate-dependent protein kinase (PKA) and calcium-dependent protein kinase (PKC) modulators on secretagogue-stimulated gastric acid secretion were studied in the continuously perfused stomach of the anesthetized rat. Intravenous histamine (0.25 mg/kg/h) and pentagastrin (2 micrograms/kg/h) increased secretion above baseline by three- and fourfold, respectively. Parenteral administration of a PKC activator, 12-o-tetradecanoylphorbol-13-acetate (TPA; 0.1 nmol/h), decreased histamine- and pentagastrin-stimulated secretion by 64 and 40%, respectively. Administration of PKC inhibitors, calphostin C and 1-(5-isoquinolinyl sulfonyl)-2 methylpiperazine (H-7; 10 nmol/h, each), increased histamine- and pentagastrin-stimulated secretion by 115 and 74% and 42 and 79%, respectively, while equimolar concentrations (10 nmol/h) of three other isoquinoline sulfonamides (HA-1004, H-8, and H-89) had no effect, except for H-89 (100 nmol/h) which inhibited the histamine- and penta-gastrin-stimulated acid secretion by 44%. Basal secretion was not significantly altered by the aforementioned drugs. The TPA-induced inhibition of pentagastrin-stimulated secretion was partially reversed by treatment with H-7. These findings support a role of PKA and PKC in the modulation of stimulated gastric acid secretion in vivo.
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PMID:Effects of cyclic adenosine monophosphate-dependent protein kinase and calcium-dependent protein kinase modulators on stimulated gastric acid secretion in the perfused rat stomach. 857 20