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)

The inhibitory action of both calcitonin (CT) and glucagon (GK) on human pancreatic secretion has been evaluated in detail. The reduction of enzyme secretion expressed as percentage corresponded to 60--80% of the initial values in response to both CT and GK when the hormones were given as single infusions during background stimulation with secretin or with secretin plus cholecystokinin-pancreozymin (CCK-PZ). After withdrawal of GK-infusion the return to normal values of enzyme secretion was distinctly faster than after CT, thus reflecting a more rapid degradation of circulating GK than of CT. In the presence of stimulation with secretin plus CCK-PZ, the combined administration of CT and GK did not enhance the inhibitory actions of CT and GK. Fluid and bicarbonate secretions were not affected by either CT or GK. The results suggest that CT and GK inhibit human pancreatic enzyme secretion by similar modes of action. Therefore, the combined administration of both CT and GK does not offer a reasonable approach to the treatment of acute pancreatitis.
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PMID:Similar modes of action of calcitonin and glucagon in inhibiting pancreatic enzyme secretion in man. 54

In anesthetized mongreal dogs, the intrarenal arterial (0.2 approximately 1.0 unit/kg-min) and the intravenous infusion (0.4 approximately 2.0 unit/kg-min) of secretin caused dose-dependent increase of RBF, accompanied by decreases of the calculated afferent arteriolar resistance (Ra) and efferent arteriolar resistance (Re), but produced no significant effect on GFR, urine flow, electrolyte excretion, osmolar clearance and free water reabsorption. The distribution of cortical blood flow was examined using the radioactive microsphere technique. The intrarenal infusion of secretin (1.0 unit/kg-min) increased renal cortical blood flow in the juxtamedullary area much more than in the superficial area, shifting the blood flow from the outer to the inner zone. Simultaneous intrarenal infusion of secretin (1.0 unit/kg-min) and glucagon (0.5 microng/kg-min) produced increases in GFR, urine flow and electrolyte excretion to a lesser degree than those induced by glucagon alone, whereas the increment in RBF and the decreases in Ra and Re were almost to the same degree as those caused by secretin alone. The present results indicate that secretin produces the dilation of afferent and efferent arterioles, resulting in an increase in RBF, with no change in GFR and urine flow, and that the effects of glucagon on renal functions are masked by secretin mainly through the effects of renal hemodynamics.
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PMID:[Effects of secretin on renal functions in the dog]. 55 40

A reliable, sensitive, reproducible and specific radioimmunoassay for cholecystokinin-pancreozymin (CCK) has been developed, using rabbit antisera to highly purified porcine hormone. The natural occurring variant of CCK (39-CCK), in which the ordinary CCK is lengthened from its N-terminus by a hexapeptide, labelled with 125J, and repurified by column chromatography on Sephadex G-10 and on SP-Sephadex C-25, was used as tracer. Separation from antibody-bound labelled 39-CCK was carried out using a double antibody procedure. Non-specific interference with the assay system was abolished by ethanol extractions. Highly purified porcine CCK was used as standard. No significant crossreaction was found with gastrin, motilin, vasoactive polypeptide (VIP), gastric inhibitory polypeptide (GIP), natural and synthetic secretin, pancreatic glucagon or insulin. The sensitivity of the assay is approximately 40 pg/ml of test solution. The mean immunoreactive CCK concentration in 45 fasting normal subjects was 222 pg/ml increasing after food ingestion to 480 pg/ml. Somatostatin was able to abolish the stimulated CCK release. Elevated CCK concentrations were found in chronic pancreatitis. Immunohistochemical identification of pancreozymin cells was carried out either in surgical samples or in biopsy material. Approximately 1650 CCK cells per cross-section in the duodenum of humans have been found. The CCK cells usually appeared elongated, oval or pyramidal in shape and were observed to reach the lumen with their apical cell pole.
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PMID:Estimation of cholecystokinin-pancreozymin (CCK) in human plasma and tissue by a specific radioimmunoassay and the immunohistochemical identification of pancreozymin-producing cells in the duodenum of humans. 56 41

The mechanism by which intestinal secretagogues evoke fluid secretion in the small bowel and colon has been suggested to involve mucosal adenylate cyclase. Adenylate cyclase activity was assayed by conversion of [32P]ATP to [32P]cyclic AMP in a system of pure epithelial cells isolated from the small intestine of the hamster by vibration in buffer. Several gastrointestinal hormones were tested for their capacity to stimulate adenylate cyclase; vasoactive intestinal peptide and impure cholecystokinin-pancreozymin (but not the 99% pure preparation or pure cholecystokinin octapeptide) were potent stimuli, but pentagastrin, glucagon, secretin, and gastric inhibitory peptide were impotent. Two prostaglandins, PGE1 and PGE2, were potent stimuli of adenylate cyclase. Two other compounds that provoke intestinal secretion of fluid, deoxycholic acid and ricinoleic acid (castor oil), were ineffective stimuli of adenylate cyclase. These experiments do not support a clear-cut relationship between a compound's ability to stimulate adenylate cylase and its activity as an intestinal secretagogue.
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PMID:Stimulation of adenylate cyclase in homogenates of isolated intestinal epithelial cells from hamsters. Effects of gastrointestinal hormones, prostaglandins, and deoxycholic and ricinoleic acids. 56 12

Seven rabbits were immunized with a synthetic C-terminal glucagon fragment [15--29] conjugated with bovine serum albumin by means of glutaraldehyde. Antisera for glucagon were produced in all the animals after six injections of the conjugate. One of them revealed a higher titer antiserum (G42), which did not cross react with gut glucagon-like immunoreactive material, secretin, insulin, gastric inhibitory polypeptide or vasoactive intestinal peptide. From the results of inhibition of 125 I-glucagon in binding with the antiserum by various glucagon-related fragments the immunogenic determinant of the antiserum was proved to be in the C-terminal residue of the glucagon molecule, although peptide [17--29] or [21--29] reacted weakly with the antiserum. The plasma glucagon levels measured by antiserum G 42 during an arginine test in five normal subjects were superposed on those obtained by other antiserum (G21), specific for pancreatic glucagon. Furthermore, a comparable standard curve for glucagon was obtained using antiserum G42, when a labelled p-hydroxyphenylacetylated glucagon fragment [15--29] was employed as a tracer. The present study clearly demonstrated that the C-terminal glucagon fragment could yield a specific antiserum for pancreatic glucagon, supporting the proposal that the C-terminal fragment of glucagon is responsible for such specific antisera. Furthermore, it is concluded that immunoassay for glucagon could be performed using the labelled glucagon fragment as a tracer.
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PMID:Production of a specific antiserum by synthetic C-terminal fragment of glucagon. 57 20

This study was undertaken to investigate the variations of the Vasoactive Intestinal Peptide (VIP) content of rat jejuno-ileum (JI) with age. VIP was measured by its ability to inhibit competitively the binding of [125I]pork VIP (pVIP) to rat liver plasma membranes. The radio receptor assay was sensitive to 0.5 ng/ml. VIP fragments 1-6, 14-28 and 18-28 exhibited no cross reaction with [125I]pVIP. Glucagon had no effect and secretin was about 100 times less effective than pVIP. Rat VIP was extracted from JI by 0.5 M acetic acid and partially purified by adsorption on silicate. The effect of JI extracts in inhibiting the binding of [125I]pVIP paralleled that of pVIP used as standard. The VIP content of JI showed a 340-fold increase between day 21 post coitum (p.c.): 41 +/- 4 ng/JI and day 63 post partum (p. p.): 14 110 +/- 954 ng/JI. On a gut weight basis, VIP increased slightly from day 21 p. c. (591 +/- 51 ng/g of JI) to day 14 p. p. (906 +/- 109 ng/g of JI) and then increased more sharply (day 21 p. p.: 1508 +/- 222 ng/g of JI) until day 63 p. p. (2672 +/- 207 ng/g of JI). The VIP content seemed to reach a plateau after 2 months. A similar pattern was observed when the results were expressed per mg of JI protein. It is speculated that the rise in VIP content is related to the role of this peptide in the regulation of the gastro-intestinal function and/or the distribution of fuels in the organism.
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PMID:Vasoactive intestinal peptide (VIP): variation of the jejuno-ileal content in the developing rat as measured by radioreceptorassay. 57 32

Endogenous insulin secretion after different stimuli was determined in insulin requiring diabetics without circulating insulin antibodies. Four groups of non-obese diabetics were investigated and compared with 111 controls. Group I: 14 patients with mild diabetes, not yet requiring insulin; diagnosis before the age of 30 years. Group II: 19 ketonuric patients just before being started on insulin treatment. Group III: 18 patients during remission after an average of 16.5 months' insulin treatment. Group IV: 13 patients with no remission period or relapse after an average of 19.5 months on insulin treatment. Blood glucose and immunoreactive insulin were measured during fasting and after iv secretin, iv tolbutamide, iv GTT, and oral GTT, followed by combined iv tolbutamide and glucagon stimulation. A considerable insulin secretion could be demonstrated in group I, whereas in group II only a very low insulin peak was obtained after secretin and the combined injection of glucagon and tolbutamide. In group III considerable insulin secretion was demonstrated, whereas in group IV only a very low insulin peak was obtained. A significant correlation between the degree of metabolic control and endogenous insulin secretion was found.
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PMID:Insulin secretion in insulin-requiring diabetics before and during insulin treatment. 57 40

Hypersecretion of gastric acid and accelerated intestinal transit are largely unexplained consequences of massive resection of the small bowel; several postulated humoral mechanisms remain unsubstantiated. The purpose of the study was to investigate the effects of 75% resection of the distal small bowel in dogs on circulating levels of a range of gastrointestinal hormones. Basal and meal-stimulated concentrations of insulin, secretin, gastrin, pancreatic glucagon, and total glucagon-like immunoreactivity (GLI) were measured by radioimmunoassay techniques. After resection, significant depletions of basal and stimulated total GLI (p less than 0.05 -- p less than 0.001) and a significant rise of stimulated gastrin (p less than 0.05) were discovered. These hormonal alterations may produce an important imbalance of humoral influences on gastrointestinal function. It is suggested that these changes may hold a key to the aetiology of the complications of massive resection of the small bowel.
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PMID:Role of gastrointestinal hormones in the response to massive resection of the small bowel. 59 Aug 47

The duodenums of opossums and cats were cut into strips 2 mm wide and 2-2.5 cm long. Strips cut in the oral-caudal axis were called longitudinal strips; those cut at 90 degrees to that axis were called circular strips. Cholecystokinin (CCK) and cerulein stimulated phasic contractions of circular muscle of opossum duodenum, but had no effect on the longitudinal muscle. The effect of CCK was not blocked by tetrodotoxin (10(-7)M), indicating a direct muscle stimulation. CCK had no effect of both muscle layers of the cat duodenum. Vasoactive intestinal peptide raised tension in longitudinal muscle, but reduced tension in circular muscle of opossum duodenum. Glucagon slightly reduced tension in both longitudinal and circular muscle of opossum duodenum. It also inhibited contractions of circular muscle caused by acetylcholine. Pentagastrin and secretin had no effect on either muscle layer in either species. These findings suggest that the circular and longitudinal muscle layers of the duodenum respond differently to at least some gastrointestinal hormones. Also, there is species variation in response to gastrointestinal hormones.
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PMID:Effects of some gastrointestinal hormones on two muscle layers of duodenum. 62 51

The effect of glucagon infusion on secretin and combined secretin and cholecystokinin stimulated exocrine pancreatic secretion was studied in normal subjects and in patients after acute and with chronic pancreatic disease. Glucagon inhibited pancreatic protein secretion and had no inhibitory effect on volume or bicarbonate secretion.
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PMID:Glucagon inhibition of secretin and combined secretin and cholecystokinin stimulated pancreatic exocrine secretion in health and disease. 62 17


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