EFFECTS OF ALPHA-2-ADRENERGIC AND BETA-ADRENERGIC AGONISM ON GLUCAGON-SECRETION FROM PERFUSED PANCREASES OF NORMAL AND STREPTOZOCIN-INDUCED DIABETIC RATS

被引:15
作者
HIROSE, H
MARUYAMA, H
ITO, K
KIDO, K
KOYAMA, K
SARUTA, T
机构
[1] Department of Internal Medicine, Keio University School of Medicine, Tokyo
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 1993年 / 42卷 / 08期
关键词
D O I
10.1016/0026-0495(93)90025-J
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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. © 1993.
引用
收藏
页码:1072 / 1076
页数:5
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