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 effect of adenosine-5'-N-ethylcarboxamide, (NECA), a long-lasting adenosine derivative with pronounced vasoactivity was investigated on glucagon and insulin release from the in situ isolated blood perfused pancreas in the anesthetized dog: NECA (10(-9) to 10(-5) mol/l) led to a dose-dependent glucagon release. Insulin release was inhibited by NECA at low concentrations, but significantly increased at higher concentrations of the adenosine analogue. Similar effects were observed with infusion of adenosine at 10(-7) and 10(-6) mol/l. Aminophylline (10(-4) mol/l) produced a 10-fold attenuation of the actions of NECA. The preponderance of glucagon release at low concentrations of NECA and adenosine in contrast to that of insulin release at high concentrations may represent a local pancreatic regulatory mechanism of adenosine in glucose homeostasis.
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PMID:The effects of NECA (adenosine-5'N-ethylcarboxamide) and of adenosine on glucagon and insulin release from the in situ isolated blood-perfused pancreas in anesthetized dogs. 675 Apr 17

The adenosine analogue 765-21 (10 micrograms/kg intravenously), substituted at the 5'-position, caused a sustained increase in plasma glucose and a decrease in plasma free fatty acid concentrations in conscious dogs. Concomitantly, plasma glucagon levels rose threefold. Changes in plasma insulin concentration were relatively small and of no statistical significance. A simultaneous fall in arterial blood pressure was also observed. Aminophylline, an adenosine antagonist, inhibited the haemodynamic as well as the metabolic responses evoked by the adenosine analogue. - In collagenase-isolated rat islets of Langerhans 765-21 inhibited glucose-induced insulin release in a dose-dependent manner (concentration range 10(-8) to 10(-5) M). In contrast to the data obtained on conscious dogs, 765-21 did not promote glucagon release from the pancreatic islets. Since stimulation of glucagon secretion was also not observed on decreasing the glucagon concentration in the incubation medium, the collagenase technique of isolation may be responsible for the insensitivity of the islets to glucagon-releasing stimuli. - The results are indicative of a specific inhibition of glucose-induced insulin release by 765-21. The data obtained in vivo additionally suggest a glucagon-releasing activity of the adenosine analogue investigated.
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PMID:[Effects of a long-acting adenosine analogue on insulin and glucagon release (author's transl)]. 700 70

The comparative activity of agonists of duodenal bicarbonate secretion was studied in the anesthetized guinea pig, where the duodenal lumen was perfused with 24 mmol/l NaHCO3 to ensure active secretion of bicarbonate. Agonists were infused alone and in combination. Dibutyryl 3',5'-cyclic adenosine monophosphate, vasoactive intestinal polypeptide (VIP) and prostaglandin E2 (PGE2) were strong stimulants of bicarbonate secretion. Theophylline, dibutyryl 3',5'-cyclic guanosine monophosphate, glucagon and prostaglandin F2 alpha (PGF2 alpha) were weaker agonists, and secretin had no effect. Combinations of any two of VIP, PGE2 and glucagon depressed bicarbonate secretion, whereas combinations of PGE2 and PGF2 alpha, VIP and PGE2, and glucagon and PGF2 alpha increased bicarbonate secretion. The data indicate that cAMP and other secondary messengers may mediate duodenal bicarbonate secretion.
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PMID:Comparative activities of agonists of active duodenal bicarbonate secretion in the guinea pig. 770 54

The effects of PACAP on hepatic glucose metabolism were examined using the flow-through perfusion method for fed rat livers, because some of the glucagon superfamily peptides stimulate hepatic glucose output. Glucose output was significantly stimulated in a dose-dependent manner by more than 1 nM PACAP-27. The potency of its stimulation was equal to that of PACAP-38, greater than that of VIP, and clearly lower than that of glucagon. The cAMP output was also increased significantly by more than 1 nM PACAP-27; however, the degree and profile of cAMP output were not in parallel with those of glucose. Theophylline did not affect these stimulatory effects. On the other hand, in the perfusion experiment with Ca2+ free perfusate, the degrees of increase in glucose output induced by 15 and 40 nM PACAP-27 were significantly reduced. In conclusion, PACAP stimulates glucose output from the perfused rat liver, and Ca2+ rather than cAMP plays an important role in this action as a second messenger.
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PMID:PACAP stimulates glucose output from the perfused rat liver. 771 74


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