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Query: UNIPROT:P01275 (
glucagon
)
26,492
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Neuroglycopenia
induced by 2-deoxy-glucose is known to activate the autonomic nervous system and to stimulate
glucagon
secretion. In this study, the relative contribution of the various branches of the autonomic nervous system on the 2-deoxy-glucose-induced
glucagon
secretion was investigated in the mouse. An intravenous injection of 2-deoxy-glucose (500 mg/kg) was followed by a 5-fold increase in plasma levels of
glucagon
(P less than 0.001). This 2-deoxy-glucose-induced
glucagon
secretion was impaired by pre-treatment with either the muscarinic antagonist methylatropine (by 83%; P less than 0.001) or the nicotinic antagonist hexamethonium (by 90%; P less than 0.001). Further, also the alpha-adrenoceptor antagonist phentolamine inhibited the
glucagon
response to 2-deoxy-glucose (by 35%; P less than 0.01). In contrast, the beta-adrenoceptor antagonist L-propranolol did not affect the
glucagon
response to 2-deoxy-glucose. It is concluded that the main mechanism behind the increased plasma levels of
glucagon
following administration of 2-deoxy-glucose is cholinergic activation. However, intact alpha-adrenoceptors are a pre-requisite for the full effect of 2-deoxy-glucose. In contrast, beta-adrenoceptors seem to be of no importance and there seems to be no room for neuropeptides as mediators of the neuroglycopenia-induced
glucagon
secretion in the mouse.
...
PMID:Inhibition of 2-deoxy-glucose-induced glucagon secretion by muscarinic and alpha-adrenoceptor blockade in the mouse. 288 9
Neuroglycopenia
induced by administration of 2-deoxy-D-glucose is known to stimulate the secretion of both insulin and
glucagon
in mice by a mechanism that is dependent on neural activity. In the present study, we examined whether the neurotransmitter nitric oxide (NO) is involved in this process. Therefore, 2-deoxy-D-glucose (500 mg/kg) was injected intravenously alone or together with the inhibitor of NO synthase, NG-nitro-L-arginine methyl ester (50 mg/kg) to conscious mice. It was found that NG-nitro-L-arginine methyl ester inhibited the increased plasma levels of both insulin (by 26%; P = 0.039) and
glucagon
(by 45%; P < 0.001) at 10 min after injection of 2-deoxy-D-glucose. Similarly, the NO synthase inhibitor, NG-nitro-L-arginine, which is devoid of the anticholinergic property of NG-nitro-L-arginine methyl ester, inhibited the responses of both insulin (by 53%; P = 0.026) and
glucagon
(by 57%; P = 0.003) to 2-deoxy-D-glucose. In contrast, the stereoisomer of NG-nitro-L-arginine methyl ester, NG-nitro-D-arginine methyl ester, which is devoid of NO synthase inhibitory activity, was without effect on 2-deoxy-D-glucose-induced insulin and
glucagon
secretion. Plasma levels of adrenaline and noradrenaline after administration of 2-deoxy-D-glucose were also reduced by NG-nitro-L-arginine methyl ester. In contrast, the insulin and
glucagon
secretory responses to intravenous injection of arginine (250 mg/kg), glucose (500 mg/kg) or the cholinergic agonist, carbachol (30 micrograms/kg), were not influenced by NG-nitro-L-arginine methyl ester, NG-nitro-D-arginine methyl ester or NG-nitro-L-arginine.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Involvement of nitric oxide in neuroglycopenia-induced insulin and glucagon secretion in the mouse. 749 51
Hypoglycemia is the most common endocrine medical emergency. Because the brain has an obligatory need for contiunous inflow of glucose, any interruption to that supply puts the individual at risk for neuroglycopenia. The latter impairs brain function and precludes self-administered corrective treatment. Treatment of hypoglycemia, especially in those patients with diabetes mellitus, involves punctilious attention to preventive measures. The acute event, if recognized, requires treatment with oral ingestion of free carbohydrate.
Neuroglycopenia
can be treated equally effectively with intravenous glucose or parenteral
glucagon
administration.
...
PMID:Hypoglycemia. 780 86