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 effects of the serotonin1A (5-HT1A) receptor agonist buspirone on the plasma glucose and pancreatic hormones insulin and glucagon were investigated in rats. Buspirone elicited significant hyperglycemia and hyperglucagonemia, although it did not affect the insulin levels. Adrenodemedullation inhibited both the increase in blood glucose and glucagon levels. These results indicate that buspirone-induced hyperglycemia and hyperglucagonemia are mediated by adrenaline release from the adrenal gland.
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PMID:The effects of the serotonin1A receptor agonist buspirone on the blood glucose and pancreatic hormones in rats. 147 42

A cDNA encoding a pituitary adenylate cyclase-activating polypeptide (PACAP) receptor was cloned from a bovine brain cDNA library using a synthetic oligonucleotide probe corresponding to the partial N-terminal amino acid sequence of the PACAP receptor purified from the bovine brain. The cloned cDNA encoded a polypeptide of 513 amino acid residues with seven putative transmembrane domains. The deduced amino acid sequence exactly matched the N-terminal amino acid sequence of the purified PACAP receptor. It also shared an apparent similarity with the vasoactive intestinal peptide (VIP), secretin, growth hormone releasing hormone, calcitonin, and glucagon receptors, suggesting that the PACAP receptor is a member of the secretin receptor subfamily of the guanine nucleotide-binding regulatory protein-coupled receptor family. Northern blot analysis showed that the size of the major mRNA band which hybridized with the cDNA was about 7 kb in the bovine cerebral-cortex and hippocampus. An expression vector containing the cloned cDNA for the PACAP receptor was introduced into Chinese hamster ovary (CHO) cells. The affinity of PACAP receptors expressed on the transfected CHO cells was quite similar to that of natural PACAP receptors on the bovine brain membranes. Competitive binding experiments showed that PACAP38 displaced the binding of 125I-labeled PACAP27 to the receptors on the CHO cells more efficiently than PACAP27, while VIP was less effective. In addition, both of PACAP27 and PACAP38 elevated the levels of cAMP and inositol phosphates in the transformed CHO cells. These results indicate that the PACAP receptors encoded by the cloned cDNA are identical to the purified PACAP receptors, and that they can stimulate dual signaling cascades.
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PMID:Cloning and expression of a complementary DNA encoding the bovine receptor for pituitary adenylate cyclase-activating polypeptide (PACAP). 804 55

Male Sprague-Dawley rats were given one of the 5-HT receptor agonists 8-OH-DPAT (0.5-2.0 mg kg-1), TFMPP (0.125-2.0 mg kg-1), DOI (0.125-2.0 mg kg-1), and m-CPBG (1.25-20.0 mg kg-1), selective for 5-HT1A, 5-HT1B, 5-HT2 and the 5-HT3 receptors, respectively, or one of the DA receptor agonists bromocriptine (2.0-32.0 mg kg-1), quinpirole (0.5-8.0 mg kg-1) and 7-OH-DPAT (0.2-3.2 mg kg-1), selective for DA D2, DA D2/D3 and DA D3 receptors, respectively. An additional group of animals was given buspirone (2.0-8.0 mg kg-1) a 5-HT1A receptor agonist and DA D2 receptor antagonist. Separate groups of rats were given both the 5-HT1A receptor antagonist pindolol and 8-OH-DPAT or both the DA D2/D3 receptor antagonist raclopride and 7-OH-DPAT. Blood samples were collected 30 min (in some cases 120 min) after drug administration and assayed for insulin, glucagon and glucose levels. The 5-HT1A receptor agonist 8-OH-DPAT produced a statistically significant decrease in plasma insulin levels and an increase in glucose, whereas glucagon levels were unaffected. The only effect observed after buspirone treatment was a small increase in plasma glucose levels. No significant effects on plasma insulin, glucagon or glucose were seen after treatment with the 5-HT1B, 5-HT2 or 5-HT3 agonists. The DA D3 receptor agonist 7-OH-DPAT produced a decrease in plasma insulin (3.2 mg kg-1, 120 min) and an increase in glucose levels. Administration of the DA D2/D3 receptor agonist quinpirole resulted only in increased plasma glucose, whereas the DA D2 receptor agonist bromocriptine had no effect. In support of a separate mediation of glucose secretion by 5-HT1A and DA D3 receptors, the effects of 8-OH-DPAT on glucose levels were antagonized by (-)pindolol pretreatment, and the 7-OH-DPAT-induced effects on glucose levels were antagonized by raclopride pretreatment. It is concluded that plasma glucose levels are under separate serotonergic and dopaminergic control, exerted via 5-HT1A and DA D3 receptors, respectively.
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PMID:Effects of selective serotonin and dopamine agonists on plasma levels of glucose, insulin and glucagon in the rat. 867 15

The effects of the 5-HT1A/1B/1D/5/7 receptor agonist, 5-carboxamidotryptamine (5-CT), on blood glucose, insulin and glucagon levels in rats were investigated. 5-CT above the dosage of 0.05 mg/kg elicited significant hyperglycemic effects and 0.1 mg/kg, induced a 35% increase in plasma glucose levels. 5-CT did not affect plasma glucagon, and serum insulin levels increased following the high dose of 5-CT. Adrenodemedullation abolished the 5-CT-induced hyperglycemia. Hyperglycemia induced by 5-CT was prevented by pretreatment with the 5-HT1/2/7 receptor antagonist, metergoline, and the 5-HT1/2/5/7 receptor antagonist, methysergide, although the 5-HT2A receptor antagonist, ketanserin, the 5-HT2A/2B/2C receptor antagonist, ritanserin, and the 5-HT3/4 receptor antagonist, tropisetron, had no effect. Although 5-CT has a high affinity with 5-HT1A receptors, the 5-HT1A and 5-HT1B and beta receptor antagonist, (-)-popranolol, did not affect 5-CT-induced hyperglycemia. These results indicate that 5-CT-induced hyperglycemia is elicited by facilitation of adrenaline release from the adrenal gland and that 5-CT-induced hyperglycemia is mediated by the 5-HT7 receptor unrelated to 5-HT1A, 5-HT1B, 5-HT2, 5-HT3, 5-HT4 or 5-HT5 receptors.
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PMID:Effects of the non-selective 5-HT receptor agonist, 5-carboxamidotryptamine, on plasma glucose levels in rats. 983 Dec 97

Effects of the 5-HT1A receptor agonist 8-hydroxy-2-di-n-(propylamino)tetralin (8-OH-DPAT) on plasma glucagon levels were investigated. 8-OH-DPAT increased plasma glucose and glucagon levels in rats. Both hyperglycemia and hyperglucagonemia elicited by 8-OH-DPAT were prevented by the 5-HT1A receptor antagonist pindolol and prior adrenodemedullation. These results suggest that increases in plasma glucagon levels induced by 8-OH-DPAT were based on the adrenaline release from the adrenal gland and its effects may contribute to its hyperglycemic effects.
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PMID:The 5-HT1A receptor agonist 8-hydroxy-2-di-n-(propylamino)tetralin (8-OH-DPAT) induces hyperglucagonemia in rats. 1164 31

Somatostatin (SST) is a cyclic polypeptide that inhibits the release of a variety of regulatory hormones (e.g. growth hormone, insulin, glucagon, thyrotropin). Moreover, SST is widely distributed within the CNS, acting both as a neurotransmitter and as a neuromodulator of other neurotransmitter systems. However, despite its extensive expression in limbic areas, and its co-localization with GABA, a neurotransmitter previously implicated in emotion, the effects of SST on anxiety and depression have not been investigated. By performing intraventricular infusions in rats we demonstrate, for the first time, that SST has anxiolytic- and antidepressant-like effects in the elevated plus-maze and forced swim test, respectively. In addition, by performing local field potential recordings of hippocampal theta activity evoked by reticular stimulation in urethane-anesthetized rats we also show that SST application suppresses the frequency of theta in a similar fashion to diazepam. This neurophysiological signature, common to all classes of anxiolytic drugs (i.e. benzodiazepines, selective 5-HT reuptake inhibitors, 5-HT1A agonists) provides strong converging evidence for the anxiolytic-like characteristics of SST. Our pharmacological antagonism experiments with bicuculline further suggest that the anxiolytic effect of SST may be attributable to the interaction of SST with GABA, whereas the antidepressant-like effect of SST may be GABA-independent. In addition to contributing to the current understanding of the role of neuropeptides in mood and emotion, these findings support a clinical role for SST (or its analogues) in the treatment of anxiety and depression.
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PMID:Anxiolytic and antidepressant effects of intracerebroventricularly administered somatostatin: behavioral and neurophysiological evidence. 1894 Feb 36

In this study, we investigated whether glucagon-like peptide-2 (GLP-2) had antidepressant-like effects in mice, and whether these activities were associated with monoamine systems in mice. Antidepressant-like effects were evaluated based on the immobility time in the forced-swim test. GLP-2 (1.5-6 microg/mouse, i.c.v.) significantly reduced the immobility time in a dose-dependent manner without affecting locomotor activity in the wheel running test and memory function in the step-down passive avoidance test. These effects were inhibited by pretreatment with metergoline (an antagonist of non-specific 5-HT receptors), parachlorophenylalanine (an inhibitor of 5-HT synthase), NAN-190 (an antagonist of 5-HT1A receptors), yohimbine hydrochloride (an antagonist of alpha2 adrenoceptors), atenolol (an antagonist of beta1 receptors), and raclopride (an antagonist of D2 receptors), but not prazosin (an antagonist of alpha1 adrenoceptors), ICI118551 (an antagonist of beta2 adrenoceptors), and SCH23394 (an antagonist of D1 receptors). These results suggest that GLP-2 exerts antidepressant-like effects in the forced-swim test in mice, which are associated with 5-HT1A, alpha2, beta1 and D2 receptors.
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PMID:Antidepressant-like effects of glucagon-like peptide-2 in mice occur via monoamine pathways. 1953 56