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)

Gastrin-releasing peptide (GRP) was infused at two dose levels [GRP I (0-30 min): bolus dose of 1.41 pmol kg-1, followed by 0.12 pmol kg-1 min-1; GRP II (30-60 min): bolus dose of 5.67 pmol kg-1, followed by 1.50 pmol kg-1 min-1] to six normal men to study the pharmacokinetics of GRP using a newly developed RIA and the effect of GRP on gastro-entero-pancreatic hormones and gastric acid secretion. The half-life of disappearance of GRP was 2.8 +/- 0.4 min (+/- SEM). The MCR and the apparent space of distribution were 33.0 +/- 4.0 ml kg-1 min-1 and 133 +/- 31 ml kg-1, respectively. GRP stimulated the secretion of gastrin, pancreatic polypeptide, insulin, glucagon, and glucose-dependent insulinotropic polypeptide in a dose-dependent manner. Gastric acid secretion was stimulated 15 min after the increase in gastrin secretion, suggesting that GRP stimulated gastric acid secretion via release of gastrin. GRP had no significant effect on the secretion of enteroglucagon or neurotensin. In the mammalian gastrointestinal tract, GRP is localized exclusively to nerve tissue. This fact and its potent effects demonstrated here make it a likely candidate for peptidergic nervous control of gastrointestinal function.
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PMID:Gastrin-releasing peptide: pharmacokinetics and effects on gastro-entero-pancreatic hormones and gastric secretion in normal men. 673 5

We have assessed the effect of omeprazole (30 mg daily) on gastric acid secretion as well as on basal hormone levels (fasting gastrin; TSH, T3, T4, TBG; insulin, glucagon, C-peptide; prolactin, testosterone, 17-beta-oestradiol, dihydroepiandrosterone, cortisol and PTH) in 8 healthy volunteers before and after a 28 day treatment. On day 29, i. e. one day after the last omeprazole dose, mean stimulated acid output was still reduced from 27.4 +/- 3.5 mmol H+/h (+/- SEM) to 7.8 +/- 1.4 mmol H+/h (72% inhibition). Fasting gastrin levels were raised from 55.5 +/- 6.8 pg/ml to 80.9 +/- 6.7 pg/ml (33% increase). On day 39, stimulated gastric acid secretion and fasting gastrin levels have been returned to pretreatment values. Basal levels of prolactin, testosterone, TSH, T3, T4, TBG, cortisol, PTH, 17-beta-oestradiol, insulin, glucagon, c-peptide, dihydroepiandrosterone remained unchanged by a 28-day omeprazole treatment. Omeprazole is a highly effective antisecretory compound without any effect on the basal hormone levels tested. Even after 28 days its effect on acid secretion and fasting gastrin levels was fully reversible.
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PMID:[4 weeks' administration of omeprazole: effect on acid behavior and basal hormone levels]. 674 Dec

Because it is known that nutrients can enhance insulin release, we studied the effect of a drink which was devoid of nutrients upon the immunoreactive insulin response to i.v. glucose in 13 normal subjects. The summated immunoreactive insulin secretory response during an i.v. glucose infusion (500 ml 10% glucose over 30 min) was 178 +/- 32 (SEM) microU/ml. However, when subjects ingested 500 ml 3% mannitol in a physiologic electrolyte solution given 30 min before the i.v. glucose, 56% augmentation of insulin release was noted (277 +/- 38 microU/ml, P less than 0.005). Post-infusion serum glucose was lower when the drink preceded i.v. glucose. The 3% mannitol-electrolyte drink itself did not significantly alter insulin, gastrin, gastric inhibitory polypeptide, or glucagonlike immunoreactivity. Two percent mannitol-electrolyte solution did not produce the insulin enhancing effects of the more hypertonic solution. In contrast with the effects of glucose, when arginine was used as the i.v. insulin secretagogue, antecedent 3% mannitol-electrolyte ingestion produced no enhancement of insulin release. This study demonstrates that ingestion of a non-nutrient drink with an osmolality of at least 456 mosmol/kg augments insulin secretion in response to a subsequent i.v. glucose load.
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PMID:Augmentation of insulin secretion by a non-nutrient drink. 676 35

Pancreatic polypeptide was infused intravenously in healthy fasting subjects at 1 pmol kg-1 (n = 7) and 4 pmol kg-1 min-1 (n = 10) producing plasma PP concentrations of 223 +/- 37 pmol/l (mean +/- SEM) and 891 +/- 64 pmol/l respectively. These levels are similar to and four-fold higher than those seen after a normal mixed breakfast in healthy young adults. In a separate study five healthy subjects ingested a small breakfast during infusion of PP on different days at 1 pmol kg-1 min-1 and 2 pmol kg-1 min-1 respectively. PP at 1 pmol kg-1 min-1 caused a marked reduction in fasting plasma motilin concentrations to 20% of the basal level (p less than 0.001). There were, however, no significant changes in plasma concentrations of insulin, glucagon, gastrin, secretin, enteroglucagon, gastric inhibitory peptide or neurotensin. Despite previous reports possibly implicating PP in metabolism, there were no significant effects on blood levels of glucose, alanine lactate, 3-hydroxybutyrate, glycerol or non-esterified fatty acids, either in the fasting state or after the ingestion of food. Although it seems unlikely that PP is a major hormonal regulator of intermediary metabolism in man, its ability to suppress motilin at physiological concentrations suggests the possibility of an indirect influence on digestive motor function.
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PMID:Effects of pancreatic polypeptide on motilin and circulating metabolites in man. 678 20

A cytochemical section-bioassay of gastrin-like activity is described in which such activity in plasma is assayed by its stimulation of carbonic anhydrase activity in serial, 18 micrometers-thick, sections of suitably prepared gastric fundus of the guinea-pig. The index of precision was 0.1 +/- 0.05 (mean +/- SEM; n=8). Fiducial limits were 75-134%. Intra-assay variation was +/- 6.4% (n=4); inter-assay variation was +/- 16.3% (n=3). The mean gastrin-like activity in the plasma of 15 fasting normal subjects was 5.1 +/- 0.49 x 10(-12)M (range 1.4-18.2 x 10(-12)M).
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PMID:The cytochemical section-bioassay of gastrin-like activity. 678 16

The plasma concentrations of gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, glucagon, and pancreatic polypeptide (PP) were studied following the ingestion of a protein rich meal in late pregnancy and postpartum in 11 normal women. In pregnancy, the fasting plasma concentrations of glucose (mean +/- SEM in pregnancy: 4.1 +/- 0.1 mmol l-1, postpartum: 4.7 +/- 0.1 mmol l-1, P less than 0.01), gut GLI (25 +/- 3 v. 33 +/- 2 pmol-eqv l-1, P less than 0.01), and PP (7.9 +/- 1.0 v. 13.0 +/- 1.2 pmol l-1, P less than 0.01) were decreased, gastrin and GIP unaltered, and insulin (90 +/- 9 v. 72 +/- 5 pmol l-1, P less than 0.05) and glucagon (17 +/- 1 v. 13 +/- 1 pmol l-1, P less than 0.01) increased. The gastrin, GIP and glucagon responses to the meal were unaffected by pregnancy, whereas the responses of gut GLI (integrated responses in pregnancy: 1217 +/- 325 pmol-eqv l-1, postpartum 2223 +/- 404 pmol-eqv l-1, P less than 0.05) and PP (9801 +/- 1440 v. 14,078 +/- 1543 pmol l-1, P less than 0.01) were impaired and the insulin response enhanced (27,973 +/- 6814 v. 11,409 +/- 3102 pmol l-1, P less than 0.01) in pregnancy. The physiological implications of these findings are at present not known in detail. They may, however, be important for the altered carbohydrate metabolism in pregnancy and also for the changes occurring during gestation in gastrointestinal physiology.
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PMID:Gastro-entero-pancreatic hormones in normal pregnancy: response to a protein rich meal. 680 Aug 4

A radioimmunochemical procedure which distinguishes sulfated from non-sulfated gastrins has been developed. Two antisera raised against synthetic non-sulfated human hexadecapeptide gastrin were used. No. 2604 binds sulfated and non-sulfated gastrins with equimolar potency, whereas No. 2605 reacts poorly with sulfated gastrin (ID50 for non-sulfated gastrin: ID50 for sulfated gastrin = 0.06). Both antisera bind gastrins of different molecular length with equimolar potency using monoiodinated human gastrin-17 as tracer. The method was validated by fractionating gastrins in serum and in tissue extracts, and by recovery experiments. We found that Component I of gastrin--like the smaller gastrin components--was present in both, sulfated and non-sulfated form. In serum from normal fasting subjects the concentration of non-sulfated gastrin was 12.5 +/- 0.8 pmol/l (mean +/- SEM) with a total range of 0-44 pmol/l and the corresponding values for sulfated gastrin were 7.5 +/- 0.5 pmol/l (range 0-20 pmol/l). Sulfated gastrin accounted for more than half of the gastrins in only 21% of normal subjects. There was a parallel rise and fall in sulfated and non-sulfated gastrins after a meal and after stimulation with adrenaline.
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PMID:Radioimmunochemical quantitation of sulfated and non-sulfated gastrins in serum. 682 8

Previous studies have questioned the physiological role of gastric inhibitory peptide in inhibiting gastric acid secretion. The present study was designed to examine and compare peptone meal-stimulated gastric acid secretion in dogs after intravenous infusion of rabbit serum containing antibodies to gastric inhibitory peptide or normal rabbit serum (as control). Five dogs were prepared with gastric fistulas. Basal acid output was collected for 90 min through the gastric fistula. After 30 min of basal acid output collection, either rabbit serum containing antibodies to gastric inhibitory peptide or normal control rabbit serum (0.1 ml/kg) was infused intravenously over 1 min. After the basal acid output collection, a 10% peptone meal was infused into the stomach. Gastric acid output was measured by intragastric titration (pH 5.0) for 60 min. Peripheral venous plasma was collected for measurement of gastrin and gastric inhibitory peptide and for binding of endogenous plasma gastric inhibitory peptide by administered antibodies to gastric inhibitory peptide before and at 2, 5, 10, 15, 30, 60, 90, and 120 min after the meal. After intravenous administration of antibodies to gastric inhibitory peptide, 98% +/- 3% (SEM) of endogenous plasma gastric inhibitory peptide was bound by administered antibodies to gastric inhibitory peptide. No binding of endogenous plasma gastric inhibitory peptide was detected after infusion of normal rabbit serum. In dogs receiving intravenous antibodies to gastric inhibitory peptide, both peptone-stimulated gastric acid output and integrated gastrin release responses were increased when compared with dogs receiving normal rabbit serum. With infusion of antibodies to gastric inhibitory peptide, there was a high degree of correlation between the increase in gastric acid output and the increase in integrated gastrin response (r = 0.900, p less than 0.04) that followed the peptone meal. This study, using antibodies to bind endogenous gastric inhibitory peptide, demonstrates the capacity of circulating gastric inhibitory peptide to inhibit meal-stimulated gastric acid secretion. Furthermore, these results support the conclusion that this enterogastrone effect of gastric inhibitory peptide is due, at least in part, to inhibition of gastrin release.
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PMID:Effects of antibodies to gastric inhibitory peptide on gastric acid secretion and gastrin release in the dog. 683 69

We compared five graded doses of decaffeinated coffee and a widely used protein test meal (Bacto-peptone) as stimulants of acid secretion (intragastric titration) and gastrin release (radioimmunoassay) in eight healthy men. In each subject, for both acid and gastrin, the sums of the responses to all five doses were greater to decaffeinated coffee than to peptone. The mean +/- SE peak acid output in millimoles per hour was 18.5 +/- 2.9 to decaffeinated coffee and 14.7 +/- 2.7 to peptone, representing 70% and 55%, respectively, of the peak acid output to pentagastrin. The mean +/- SEM peak increment over basal rate in serum gastrin in picograms per milliliter was 84.8 +/- 4.4 to decaffeinated coffee and 44.8 +/- 2.1 to peptone. At equal concentrations, decaffeinated coffee was a more potent stimulant of acid secretion and of gastrin release than peptone. The ingredient(s) of decaffeinated coffee that accounts for its high potency in stimulating acid secretion and gastrin release has not been identified.
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PMID:Gastric acid and gastrin response to decaffeinated coffee and a peptone meal. 689 24

Synthetic neurotensin was infused into five healthy subjects at a mean dose of 2.3 pmol/kg . min for 30 min, producing a rise in plasma neurotensin concentrations, measured by RIA of 104 +/- 10 (mean +/- SEM) pmol/liter. The mean disappearance half-time on stopping the infusion was 3.8 +/- 0.2 min. The MCR was 16 +/- 1 ml/kg . min, and the apparent space of distribution was 88 +/- 6 ml/kg. During the neurotensin infusions, plasma pancreatic polypeptide rose by 145 +/- 54 pmol/liter. In contrast to results in experimental animals, there was no significant change in the pulse or blood pressure of the subjects or any significant change in blood glucose or plasma concentrations of insulin, glucagon, gastric inhibitory peptide, gastrin, motilin, or vasoactive intestinal peptide. Similarly, there was no change in plasma concentrations of TSH, GH, PRL, LH, and FSH.
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PMID:Neurotensin infusion in man: pharmacokinetics and effect on gastrointestinal and pituitary hormones. 700 47


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