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大鼠胰岛素诱导低血糖期间反调节激素的协同作用:脂解和糖异生对高血糖的参与。

Synergistic effect of counterregulatory hormones during insulin-induced hypoglycemia in rats: participation of lipolysis and gluconeogenesis to hyperglycemia.

作者信息

Souza H M, Hell N S, Lopes G, Bazotte R B

机构信息

Departamento de Ciências Fisiológicas, Universidade Estadual de Londrina, PR, Brazil.

出版信息

Zhongguo Yao Li Xue Bao. 1996 Sep;17(5):455-9.

PMID:9863174
Abstract

AIM

To study the synergistic effect of G (glucagon, 0.02 mg.kg-1), H (hydrocortisone, 20 mg.kg-1) and E (phenylephrine + isoproterenol, both 1 mg.kg-1) during insulin-induced hypoglycemia (IIH) in rats with 6 h of food deprivation (F6 group).

METHODS

I (insulin, 1 U.kg-1) was injected i.p. and 30 min later saline (F6 + I group), H, G and E individually or combined (G + H, G + E, H + E and G + H + E) were all injected i.p. and all experiments started 1 h after I injection.

RESULTS

The rise in glycemia with H + G + E was greater than the sum of the responses to i.p. H, G and E individually or in double combination plus any single hormone. This effect was reproduced by G + H + Iso (isoproterenol, 1 mg.kg-1), G + H + Iso + Met (metoprolol, 1 mg.kg-1) and G + H + Sal (salbutamol, 1 mg.kg-1). A clear relationship was shown between glycemia and free fatty acids levels. Liver gluconeogenesis from glycerol (2 mmol.L-1) was higher in the group which received G + H + beta-adrenergic agonist vs control rats (F6 or F6 + I groups).

CONCLUSION

(a) Acute hyperglycemia is obtained from a condition of IIH by combined i.p. of G + H + beta-adrenergic agonists; (b) This effect cannot be ascribed to a single hormone, but is a consequence of the combined effects of these substances; (c) Blood insulin levels and liver glycogen have no participation; (d) Lipolysis mediated by a beta-adrenergic mechanism and gluconeogenesis from glycerol contribute to the hyperglycemia.

摘要

目的

研究在禁食6小时的大鼠(F6组)胰岛素诱导的低血糖症(IIH)期间,胰高血糖素(G,0.02mg·kg-1)、氢化可的松(H,20mg·kg-1)和去氧肾上腺素+异丙肾上腺素(E,均为1mg·kg-1)的协同作用。

方法

腹腔注射胰岛素(I,1U·kg-1),30分钟后分别腹腔注射生理盐水(F6+I组)、H、G、E或其组合(G+H、G+E、H+E和G+H+E),所有实验在注射I后1小时开始。

结果

H+G+E使血糖升高的幅度大于单独腹腔注射H、G、E或其两两组合再加任何一种单一激素时的反应之和。G+H+异丙肾上腺素(异丙肾上腺素,1mg·kg-1)、G+H+异丙肾上腺素+美托洛尔(美托洛尔,1mg·kg-1)和G+H+沙丁胺醇(沙丁胺醇,1mg·kg-1)也产生了这种效应。血糖与游离脂肪酸水平之间呈现明显的关系。与对照大鼠(F6或F6+I组)相比,接受G+H+β-肾上腺素能激动剂的组中,由甘油(2mmol·L-1)进行的肝脏糖异生作用更高。

结论

(a)通过腹腔注射G+H+β-肾上腺素能激动剂可在IIH状态下实现急性高血糖;(b)这种效应不能归因于单一激素,而是这些物质联合作用的结果;(c)血液胰岛素水平和肝糖原不参与其中;(d)由β-肾上腺素能机制介导的脂肪分解和由甘油进行的糖异生作用促成了高血糖。

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Synergistic effect of counterregulatory hormones during insulin-induced hypoglycemia in rats: participation of lipolysis and gluconeogenesis to hyperglycemia.大鼠胰岛素诱导低血糖期间反调节激素的协同作用:脂解和糖异生对高血糖的参与。
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