Effects of alpha 2- and beta-adrenergic agonism on glucagon secretion from perfused pancreata of normal and streptozocin-induced diabetic rats.
Metabolism
; 42(8): 1072-6, 1993 Aug.
Article
en En
| MEDLINE
| ID: mdl-8102194
ABSTRACT
Insulin secretion is known to be inhibited by alpha 2-adrenergic agonism and stimulated by beta-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 alpha 2- and beta-adrenergic agonism on islet alpha cells, using isolated perfused pancreata of normal and streptozocin-induced diabetic (STZ-D) rats. The alpha 2-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 beta-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 alpha 2- and beta-agonistic effects were almost completely inhibited in the presence of the alpha 2-adrenoceptor antagonist yohimbine and the beta-adrenoceptor antagonist 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 beta- but also also alpha 2-adrenergic agonism stimulates glucagon secretion from rat pancreatic alpha cells.
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Banco de datos:
MEDLINE
Asunto principal:
Páncreas
/
Glucagón
/
Agonistas alfa-Adrenérgicos
/
Agonistas Adrenérgicos beta
/
Diabetes Mellitus Experimental
Límite:
Animals
Idioma:
En
Revista:
Metabolism
Año:
1993
Tipo del documento:
Article
País de afiliación:
Japón