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)

Six healthy volunteers received a 60 min infusion of guanfacine (alpha 2-agonist) on two occasions, preceded by either idazoxan (alpha 2-antagonist) or vehicle. Idazoxan elevated blood pressure by 8/7 mmHg, but there was no change on either day during guanfacine infusion. Guanfacine reduced plasma noradrenaline by approximately 30%, and this was not antagonized by idazoxan. By contrast, the 30-fold increase in plasma growth hormone caused by guanfacine was almost completely blocked by idazoxan. Guanfacine caused a two- to three-fold increase in plasma glucagon and a similar reduction in plasma insulin. Only the latter was antagonized by idazoxan. No consistent changes in plasma ACTH were observed after either idazoxan or guanfacine. Idazoxan itself elevated plasma noradrenaline up to twice baseline values, but did not affect the other metabolic measurements. alpha 2-Adrenoceptor stimulation plays a minor role in control of hormone release but has a greater physiological role in regulating release of the neurotransmitter, noradrenaline.
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PMID:Metabolic and haemodynamic effects of alpha 2-adrenoceptor stimulation and antagonism in man. 285 10

The aim of the present study was to evaluate the effect of the alpha 2-adrenoceptor antagonist idazoxan on hormonal responses and hypoglycaemia symptoms in patients with insulin-dependent (Type 1) diabetes mellitus. Six male Type 1 diabetic patients were studied with and without intravenous infusion of idazoxan. Hypoglycaemia was induced by an intravenous infusion of insulin (100 mU.kg-1.h-1), together with a glucose clamp, to obtain an arterialised venous blood glucose level of 2.3 mmol/l. Idazoxan was given at a dose of 295 micrograms/kg. Venous blood samples were obtained for analyses of free insulin, growth hormone (GH), glucagon and catecholamines. Symptoms were scored on a visual-analogue rating scale. Areas under the curves with and without idazoxan were respectively 22.4 +/- 7.0 vs 33.0 +/- 9.6 micrograms.l-1.h (p = 0.17) for GH, 4.1 +/- 1.1 vs 2.4 +/- 0.9 nmol.l-1h (p < 0.05) for adrenaline, 5.6 +/- 0.9 vs 1.3 +/- 0.5 nmol.l-1.h (p < 0.05) for noradrenaline and 51 +/- 38 vs -40 +/- 11 ng.l-1.h (p < 0.05) for glucagon. Sweating and palpitations were more pronounced during idazoxan infusion than during the control test. It is concluded that idazoxan increases catecholamine and glucagon responses as well as some of the warning signals of hypoglycaemia in Type 1 diabetic patients, whereas the GH response seems less affected by idazoxan.
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PMID:Acute effects of the alpha 2-adrenoreceptor antagonist idazoxan on hormonal responses and symptoms of hypoglycaemia in patients with type 1 diabetes mellitus. 869 93

The study purpose was to investigate the direct effect of amitraz, a formamidine insecticide/acaricide, and its active metabolite BTS 27271 on insulin and glucagon secretion from the perfused rat pancreas. Amitraz and BTS 27271 (0.01, 0.1, 1, and 10 micromol/L) inhibited insulin secretion in a concentration-dependent manner. Amitraz increased glucagon secretion at 10 micromol/L, whereas BTS 27271 increased glucagon secretion at 1 and 10 micromol/L. Amitraz- and BTS 27271-induced decreases in insulin secretion and increases in glucagon secretion were not abolished during the 10-minute washout period. During the arginine treatment, both amitraz and BTS 27271 groups (0.1, 1, and 10 micromol/L) had lower insulin secretion and higher glucagon secretion than the control group. Idazoxan, an alpha2A/2D-adrenergic receptor (AR) antagonist, prevented the inhibitory effect of amitraz on insulin secretion in a concentration-dependent manner, but prazosin, an alpha1- and alpha2B/2C-AR antagonist, failed to antagonize the effect of amitraz. These results demonstrate that (1) amitraz and BTS 27271 inhibit insulin and stimulate glucagon secretion from the perfused rat pancreas, (2) amitraz inhibits insulin secretion by activation of alpha2D-ARs, since rats have alpha2D- but not alpha2A-ARs, and (3) amitraz and BTS 27271 may have a high binding affinity to the alpha2D-ARs of pancreatic islets.
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PMID:Effects of the pesticide amitraz and its metabolite BTS 27271 on insulin and glucagon secretion from the perfused rat pancreas: involvement of alpha2D-adrenergic receptors. 1058 58