Effects of α2- and β-adrenergic agonism on glucagon secretion from perfused pancreata of normal and streptozocin-induced diabetic rats

Hiroshi Hirose, Hiroshi Maruyama, Katsuhiko Ito, Koichi Kido, Kazunori Koyama, Takao Saruta

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Abstract

Insulin secretion is known to be inhibited by α2-adrenergic agonism and stimulated by β-adrenergic agonism in both experimental animals and humans. In contrast, adrenergic regulation of glucagon secretion remains controversial. This study was designed to determine the effects of α2- and β-adrenergic agonism on islet α cells, using isolated perfused pancreata of normal and streptozocin-induced diabetic (STZ-D) rats. The α2-adrenoceptor agonist clonidine at a concentration of 10-7 mol/L significantly stimulated glucagon secretion as compared with basal levels in both normal (1,286 ± 90 v 417 ± 53 ng/L, P < .01) and STZ-D rats (551 ± 86 v 130 ± 19 ng/L, P < .01). Also, the β-adrenoceptor agonist isoproterenol at a concentration of 10-7 mol/L significantly stimulated glucagon secretion as compared with basal levels in both normal (751 ± 130 v 347 ± 41 ng/L, P < .05) and STZ-D rats (182 ± 22 v 92 ± 20 ng/L, P < .01). Furthermore, these α2- and β-agonistic effects were almost completely inhibited in the presence of the α2-adrenoceptor antagonist yohimbine and the β-agonistic effects were almost propranolol at a concentration of 10-6 mol/L, respectively. Insulin secretion was markedly reduced in STZ-D rats. These results suggest that even in a severely diabetic state, not only β- but also α2-adrenergic agonism stimulates glucagon secretion from rat pancreatic α cells.

Original languageEnglish
Pages (from-to)1072-1076
Number of pages5
JournalMetabolism
Volume42
Issue number8
DOIs
Publication statusPublished - 1993 Aug

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ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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