Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Carbonized microspheres, 15 mu in diameter and labelled with 85Sr or 51Cr were injected into the left ventricle of unanesthetized male rats to investigate the changes induced by secretin and glucagon in the distribution of cardiac output to various organs including splanchnic organs. Secretin (0.5 U/100 g i.v.) significantly increased the cardiac output distribution to the stomach, small intestine and pancreas, while the percentage distribution of the cardiac output to the heart, lungs and kidneys was unchanged. On the other hand, glucagon (10 microgram/100 g i.v.) significantly increased the cardiac output distribution to the heart, lungs and kidneys, while the distribution to the major splanchnic organs remained unchanged with the exception of hepatic arterial perfusion which was significantly increased by glucagon.
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PMID:Differences in the effects of secretin and glucagon on the blood circulation of unanesthetized rats. 72 16

Antibody was readily produced in a rabbit against synthetic porcine secretin coupled to BSA. The final dilution of the antiserum to bind 50% of 1 fmol 125I-labeled secretin was 1 : 150,000. The effective equilibrium constant (Keff) according to Scatchard was 3.4 X 10(11) l/mol, the average equilibrium constant (Ko) according to Sips 3.5 X 10(11) l/mol, and the index of heterogeneity (alpha) according to Sips 1,00. No cross reactivity was found for gastrin, glucagon and insulin. 125I-labeled synthetic porcine secretin was prepared by the Chloramine-T-method, and the label purified on a Sephadex G-15 column followed by a SP Sephadex C-25 column had a specific radioactivity of 1.150 muCi/nmol. The radioimmunoassay method described has a detection limit of 1.6 pmol/l with 95% confidence limit, a within assay precision of 9,6%, and a between assay precision of 12.8%. It allows detection of fasting plasma secretin in the low pmol/l range, and the rather sharp rise and fall in plasma secretin subsequent to a brief period of duodenal acidification. The problem involved in measuring plasma secretin have been overcome by acidification of the plasma, and by subtracting the "apparent" secretin concentration in corresponding secretin-free plasma prepared by incubation at 37 degrees C for 96 h for each subject.
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PMID:Radioimmunoassay of secretin in acidified plasma. 72 17

In 10 duodenal ulcer patients gastric acid secretion was stimulated by intravenous infusion of 1.5 microgram pentagastrin per kilogram hour. When acid secretion had reached a plateau, glucagon in a dose of 30 microgram per kilogram hour, secretin in a dose of 1 IU per kilogram hour or caerulein in a dose of 0.1 microgram per kilogram hour were infused into a separate vein for one hour during the intravenous infusion of pentagastrin. Using these doses, each drug produced about 30 per cent inhibition given separately. The highest degree of inhibition was obtained by the combination of glucagon and secretin. The inhibition reached the sum of the inhibitions after glucagon and secretin administered separately. Caerulein added to glucagon or secretin could slightly increase the inhibitory effect of these drugs given separately. Caerulein, however, failed to increase inhibition when glucagon and secretin were infused simultaneously.
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PMID:Inhibitory effect of glucagon, secretin and caerulein on gastric acid secretion stimulated by pentagastrin in patients with duodenal ulcer. 72 19

Fasting levels of 5 gut hormones were studied in 30 patients with advanced uraemia (CRF), 40 undergoing regular dialysis (RD) and 555 renal transplant patients (RT). Mean values of gastrin and total glucagon were markedly elevated in CRF and RD patients compared with 20 normal subjects; there were lesser elevations in pancreatic glucagon, insulin and vasoactive intestinal peptide (VIP). Secretin levels were unchanged. In RT patients, fasting levels of VIP and pancreatic glucagon had returned to normal, while levels of gastrin, total glucagon and insulin remained slightly elevated compared with controls. Food stimulated hormone levels were measured in 18 RD patients and compared with 18 controls. After eating, RD patients failed to show the late increase in total glucagon, or the suppression of VIP and secretin seen in normal subjects; the pattern of gastrin and insulin response was similar to controls, but after the initial increase plasma levels in RD patients tended to show a slower decline. Thus involvement of the gastrointestinal tract in uraemia is associated with functional disturbance of the endocrine system of the gut.
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PMID:Elevations of gastrointestinal hormones in chronic renal failure. 74 Jun 78

To investigate the effect of physiological doses of secretin on pancreatic A and B cell functions, secretin was infused at a rate of 0.5, 1.0 and 2.0 clinical unit per kg body weight per hr into eight normal men for 30 min or 60 min after an over-night fast, and changes in plasma immunoreactive insulin (IRI) and glucagon immunoreactivity (GI) were measured while monitoring circulating secretin levels by a radioimmunoassay. During the infusion of secretin, the plasma immunoreactive secretin (IRS) levels rose to 140-390 pg/ml which was within a range of the physiological fluctuation in plasma secretin levels reported hitherto. No significant alteration of plasma IRI and GI levels could be demonstrated during these simulated physiologic infusions of secretin. These data suggest that, in humans, the physiological dose of secretin does not influence insulin and glucagon secretion from the pancreas in the basal state.
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PMID:Effect of secretin on plasma insulin and glucagon in man. 74 71

A new model of a reversible long-term pancreatic fistula was used on an alert, unrestrained dog to test the effect of four substances of the GEP system on the exocrine pancreatic function. The results indicate that SST significantly inhibits not only the basal secretion but also the stimulated secretion of volume, bicarbonate, and trypsine. Calcitonine inhibits only the stimulated secretion whereas PGE1 inhibits only the secretin-stimulated output of trypsine. Glucagon inhibits secretin stimulation in all three parameters.
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PMID:[Long-term study of endocrine inhibition of exocrine pancreas secretion in the conscious dog]. 75 88

It has previously been shown that dopamine stimulates pancreatic exocine secretion and inhibits acid secretion in the dog. In this study, the authors have investigated the effect of dopamine on human gastric and pancreatic secretions. In 6 subjects, dopamine produced a dose-dependent inhibition of pentagastrin-stimulated acid secretion, an effect that was suppressed when the subjects received haloperidol. In 6 other subjects, dopamine infusion did not modify basal pancreatic secretion, and dopamine inhibited pancreatic enzyme secretion during secretin-cholecystokinin infusion. Dopamine also caused a rise in plasma glucagon and insulin. The effects on pancreatic enzyme secretion and plasma glucagon were not antagonized by haloperidol. The results suggest that dopamine is inhibitory for human gastric secretion. The authors did not observe a stimulatory effect of dopamine on human pancreatic exocrine secretion as has been observed in dogs.
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PMID:Effect of dopamine on human gastric and pancreatic secretion. 75 61

1. The peptic responses to Boots, GIH and synthetic secretins have been compared in fasting anaesthetized cats in which the pylorus and bile duct were occluded to prevent the release of duodenal hormones by acid and bile salts. A quantity of dilute acid introduced into the stomach at regular intervals ensured the total recovery of viscid secretions and preserved peptic activity. 2. The mean peak outputs of pepsin obtained in response to Boots secretin were significantly greater than the mean peak outputs of pepsin stimulated by equipotent doses of GIH secretin (4 Crick-Harper-Raper units of Boots secretin have been shown to stimulate a flow of juice and bicarbonate from the pancreas equal to that produced by 1 clinical unit of GIH secretin). The maximum output of pepsin stimulated by Boots secretin, 16 C.H.R. u./kg hr was 3 times the observed maximum output in response to the 4 times more potent dose of GIH secretin, 16 c.u./kg hr. The slopes of the log dose-response lines were significantly different for these two products indicating that their modes of action in stimulating pepsin may not be identical. 3. The outputs of pepsin following GIH and synthetic secretin were similar. Both these secretins stimulated the secretion of pepsin when infused in doses which stimulated the pancreas supramaximally. The less pure product Boots secretin evoked significantly higher peptic responses at doses submaximal for pancreatic stimulation, suggesting that a substance other than secretin exists in Boots preparations which contributes significantly to the overall output of pepsin in response to this product. The peptic response which was accompanied by a slight increase in acid output, but without any increase in pancreatic lipolytic activity, was not inhibited by atropine. This substance which is not present in highly purified GIH secretin does not appear to be cholic acid, gastrin, pancreozymin, glucagon or insulin. 4. The possibility that a vasodilator substance is present in Boots secretin which by expanding the splanchnic bed increases the concentration of secretin at target sites in the stomach and pancreas seems unlikely, as the flow of pancreatic juice does not increase proportionately with the vast increase in pepsin. A vasodilator substance which specifically affects the gastric vasculature remains a theoretical but unlikely explanation for our observation.
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PMID:A comparison of the pepsin stimulating effects of secretin preparations. 78 Dec 17

Immunofluorescent cells to synthetic secretin were identified in monolayer culture of neonatal rat pancreas. No cross reaction of anti-secretin was observed with either glucagon, somatostatin or gastrin. The presence of cells containing secretin or a secretin-like peptide adds a new cell type to the three already characterized (insulin, glucagon and somatostatin containing cells) in monolayer culture.
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PMID:Immunofluorescent localization of secretin in pancreatic monolayer culture. 78 98

Gastrin- and cholecystokinin (C.C.K.)-containing cells were detected by using anti-gastrin and anti-C.C.K. sera in the gastrointestinal tract of human fetuses and premature infants and in the stomach and duodenum of adult man obtained by biopsy from eight patients with normal gastro-duodenal endoscopy. The specificity of immunocytological reactions was ascertained by studying the inhibition of the reaction by gastrin, C.C.K., secretin, somatostatin, glucagon, insulin, serotonin, histamin, caerulein and octapeptide of C.C.K. In adult man, the gastrin cells are located only in the antrum and juxtapyloric region; C.C.K. was detected in the duodenum. In the human fetus, the first gastrin cells are seen in the antrum at 14 weeks of age and in the duodenum as early as 10 weeks; the C.C.K. cells are seen in the small intestine at 10 weeks of age.
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PMID:Identification of gastrin-secreting cells and cholecystokinin-secreting cells in the gastrointestinal tract of the human fetus and adult man. 79 24


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