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)

Secretin stimulates insulin release directly and augments insulin responses when administered prior to an insulinogenic stimulus. The magnitude and specificity of this augmentation effect of secretin pretreatment was evaluated in normal subjects to pulses of the following stimuli: 5 g glucose (n = 6), 1 g arginine (n = 8), 2 microgram isoproterenol (n = 6), 0.5 g tolbutamide (n = 5) and 0.5 mg glucagon (n = 6). Secretin was administered either as a 15 U pulse with a 3 U/min infusion for 25 min or as 4-150 U pulses. A period of 30 min elapsed after either the cessation of the infusion or the final 150 U pulse. In all studies, the acute insulin responses immediately following secretin were observed and had returned to baseline levels prior to the administration of any insulinogenic stimulus. Secretin only augmented the acute insulin responses to 5 g glucose pulses (pre-secretin glucose; 28 +/- 20 muU/ml, mean +/- SD; post-secretin glucose pulse: 45 +/- 37 muU/ml, P less than 0.5), an increase of 56 +/- 21% (P less than .005). A highly linear relationship was noted (r = .98, P less than .01) between the acute insulin response to glucose before and after secretin suggesting that the insulin response to the control glucose pulse is a major determinant of the glucose stimulated response after secretin. Secretin pretreatment did not augment the insulin responses to arginine, isoproterenol, tolbutamide and glucagon. The specificity of secretin for augmenting glucose stimulated insulin release suggets a possible role for secretin in carbohydrate metabolism.
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PMID:The augmentation effects of secretin on the insulin responses to known stimuli: specificity for glucose. 87 55

The effects on gallbladder contraction of three structurally related peptides, secretin, glucagon and the vasoactive intestinal peptide (VIP) have been compared in urethane-anesthetized guinea pigs. Secretin and glucagon had no effect alone but augmented cholecystokinin (CCK)-induced contractions. VIP decreased CCK-induced contractions.
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PMID:Effect of secretin, glucagon and VIP on gallbladder contraction. 95 25

1. The effects of secretin on inotropic and chronotropic activity were investigated in nine isolated canine atrium preparations which were suspended in a bath and perfused with arterial blood from a carotid artery of a heparinized donor dog. 2. Secretin administered into the cannulated sinus node artery in a dose range of 0-1-10 units produced a dose-related positive inotropic and a biphasic chronotropic effect. 3. The positive chronotropic and inotropic responses to secretin were not suppressed by treatment with alprenolol in doses which blocked responses to noradrenaline. 4. The negative chronotropic response to secretin was not blocked by atropine in doses which blocked the response to acetylcholine. 5. After treatment with glucagon, secretin produced dose-related negative chronotropic and a positive inotropic effects. Thus glucagon may antagonize the positive chronotropic effect of secretin. 6. From these results, it is concluded that secretin has a direct effect on atrial rate and contractility.
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PMID:Effect of secretin on pacemaker activity and contractility in the isolated blood-perfused atrium of the dog. 97 12

Restraint stress ulcers in rats were developed and procedures evaluated designed at preservation of intact gastric microcirculation (pO2). Neither prior truncal vagotomy, splanchnicotomy nor combined dissection of abdominal autonomic nerves were effective in preventing the stress mediated fall of mucosal pO2 and the rise in plasma glucagon. The ulcer index remained elevated and gastrin essentially was unchanged. Prophylactic injection of increasing doses (1, 2, 4, 8, 16 U/kg secretin maintained microcirculation at pO2-levels subnormal for unstressed animals (Vmax 15.53 mm Hg; Km. 0.99 U/kg), but simultaneously brought about a continuous rise in serum gastrin. Up to 8 U/kg plasma glucagon was higher than in saline control groups reaching a peak value with 2 U/kg when ucler index showed its nadir. Secretin therapy (4, 8 U/kg) markedly improves both mucosal pO2 and ulcer index. It is suggested that breakdown of gastric microcirculation may not be solely responsible for stress ulcer development.
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PMID:Rat gastric mucosal oxygen tension, ulcer index, plasma gastrin and glucagon following restraint stress. Influence of vagotomy, splanchnicotomy and exogenous secretin. 98 7

The action of duodenal acidification, of continuous I.V. infusion of secretin and glucagon and of a one bolus I.V. administration of secretin and glucagon at maximal doses on BBS-induced gastrin secretion has been studied in a group of 18 healthy subjects. Continuous infusion of secretin and glucagon and the acidification of the duodenum did not alter significantly the levels of gastrin stimulated by BBS. Secretin and glucagon administered by a single I.V. bolus paritially inhibit the effect of BBS on gastrin levels. On the basis of these results it is not possible to affirm or to exclude the possibility that BBS is a hormone physiologically present in man.
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PMID:Effect of secretin, glucagon and duodenal acidification on bombesin-induced hypergastrinemia in man. 100 44

Mongrel dogs were prepared by cholecystectomy, ligation of the lesser pancreatic duct, and insertion of modified Thomas cannulas into the duodenum and stomach. After recovery from surgery, experiments were performed by cannulation of the common bile duct for bile collection through the duodenal cannula. Bile flow and composition and the biliary clearance of erythritol were observed during secretin, glucagon, or sodium taurocholate choleresis and were compared with control studies. All test substances caused increased bile secretion. Sodium taurocholate caused a marked increase in bile salt output and in the biliary clearance of erythritol. Secretin caused a large increase in bile flow, no increase in bile salt output, and a very small increase in the biliary clearance of erythritol. The results indicate marked differences in the choleretic mechanism of sodium taurocholate and secretin and suggest that the principal action of taurocholate was on the canaliculi and the principal action of secretin was on the ducts.
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PMID:The choleretic mechanisms of sodium taurocholate, secretin, and glucagon. 114 27

COOH-terminal octapeptide of cholecystokinin (CCK-octapeptide) and the cholinergic agent carbamylcholine each produced a fourfold stimulation of calcium outflux in guinea pig isolated pancreatic acinar cells. Neither agent altered calcium influx. Stimulation of calcium outflux was rapid and specific, was abolished by reducing the incubation temperature to 4 degrees C, and was a saturable function of the secretagogue concentration. The concentrations of CCK-octapeptide and carbamylcholine that produced half-maximal stimulation of calcium outflux were 3.1 x 10(-10) M and 4.9 x 10(-5) M, respectively. The cholinergic antagonist antropine competitively inhibited carbamylcholine stimulation of calcium outflux but did not alter stimulation produced by CCK-octapeptide. Stimulation of calcium outflux by maximal concentrations of carbamycholine plus CCK-octapeptide was the same as that produced by a maximal concentration of either agent alone.Calcium outflux became refractory to stimulation by secretagogues, and incubation with either CCK-ostapeptide or carbamylcholine produced a refractoriness to both agents. The relative potencies with CCK and its related fragments stimulated calcium outflux were CCK-octapeptide greater than heptapeptide greater than CCK greater than hexapeptide = gastrin. Secretin, glucagon, and vasoactive intestinal peptide, at concentrations as high as 10(-5) M, failed to alter calcium outflux and did not affect stimulation by CCK-octapeptide or by carbamycholine.
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PMID:Action of cholecystokinin and cholinergic agents on calcium transport in isolated pancreatic acinar cells. 115 Aug 77

Effects of intravenous (IV) infusion of secretin during IV infusion of glucose were examined in normal men. Secretin was administered according to three schedules: with each schedule a comparable priming dose was delivered in the first minute, but this was followed by a maintained (120 min) infusion of secretin at a relatively high rate, or by maintained infusion at one-third that rate, or by brief (15 min) infusion at the lower rate. The lower infusion rate produced increments in secretin in the blood within the range attainable during endogenous secretion. By comparison with effects of glucose alone each secretin infusion enhanced the increments of immunoreactive insulin in the blood. Enhancement of the early release (0-5 min) of insulin was similar with each type of secretin infusion, but the integrated changes in insulin levels through the total infusion period were related to the total doses of secretin. With each dose of secretin glucose tolerance was improved but the three mean glucose curves observed during infusions of secretin were not distinguishable from one another in spite of widely different integrated insulin responses. Secretin did not modify suppression of immunoreactive glucagon or free fatty acids in the blood during hyperglycemia. The results suggest that the effect of continuous administration of secretin on glucose tolerance is not simply related to its integrated insulinotropic action. It is suggested that the effect may be highly dependent on enhancement of insulin secretion early in the response to glycemia, or that it may be due to effects of secretin on glucose production or disposal which are not mediated by insulin.
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PMID:Effects of secretin on insulin secretion and glucose tolerance. 122 79

We have documented and characterized the down-regulation of the 125I-secretin binding sites and the associated desensitization of the secretin receptor-cAMP system in rat gastric glands. Secretin induced a rapid decrease of the high-affinity 125I-secretin binding sites with t1/2 = 30 min at 37 degrees C. Half-maximal down-regulation and desensitization occurred at 10(-9) M secretin, a physiological concentration corresponding to the half-maximal activation of the secretin receptor. The Scatchard parameters of the low-affinity 125I-secretin binding sites were unaffected by the pretreatment. This desensitization is heterologous in view of the loss of responsiveness to the truncated glucagon-like peptide 1 (TGLP-1), and pharmacologically selective since the secretin-related analogue VIP (10(-7) M) does not alter the secretin-induced cAMP generation in rat gastric glands. The glycoprotein nature of the secretin receptor has also been demonstrated using WGA-agarose affinity chromatography of the solubilized 125I-secretin receptor complex.
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PMID:Functional and structural characterization of the secretin receptors in rat gastric glands: desensitization and glycoprotein nature. 165 Jun 11

In this study was observed the influence of Pancreozymin, Secretin, Glucagon, Pentagastrin and Somatostatin on the motility of duodenum in 256 seances in acute experiments on 12 dogs before and after truncal vagotomy and on 20 Wistar rats. As a control we used the return of the parameters of electrical and motor activity to their original levels. The reaction was registered with the help of electromyography, using bipolar electrodes and with measurement of intraluminal pressure, using open-tip catheter technique. Spike-activity was graphically presented and statistically performed. It was shown, that Secretin and Glucagon caused relaxation of duodenum, but Pentagastrin, Pancreozymin and Somatostatin stimulated duodenal motility with spastic component and gradual phasic character of a process. After truncular vagotomy the reaction to Pancreozymin and Pentagastrin was slowly, to Glucagon strongly reduced, but the reaction to Secretin was extended. We observed after TV either no reaction or a diminished reaction to Somatostatin. This study serves as experimental basis for use of gastrointestinal hormones and electromyography for diagnosis and therapy of motility disorders of duodenum in surgical practice.
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PMID:[Effect of gastrointestinal hormones on duodenal motility in acute experiments]. 168 2


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