Details

Autor(en) / Beteiligte

• Fóscolo, Rodrigo Bastos
• de Castro, Mauricio Gustavo Bravim
• Marubayashi, Umeko
• dos Reis, Adelina Martha
• Coimbra, Cândido Celso

Titel

Medial preoptic area adrenergic receptors modulate glycemia and insulinemia in freely moving rats

Ist Teil von

• Brain research, 2003-09, Vol.985 (1), p.56-64

Ort / Verlag

London: Elsevier B.V

Erscheinungsjahr

2003

Quelle

MEDLINE

Beschreibungen/Notizen

• In order to investigate the role of medial preoptic area (MPOA) adrenoceptors in regulation of plasma glucose and insulin secretion, we injected 40 nmol of noradrenaline, clonidine or isoproterenol into the MPOA of freely moving Wistar rats. The animals were fitted with chronic jugular catheters for blood sampling and unilateral intracerebral cannulae placed into MPOA. The results showed that noradrenaline injection into MPOA produced a rapid increase in plasma glucose levels and insulin secretion, reaching a peak at 15 min post stimulus (25% over basal, P<0.01) for plasma glucose and at 30 min for insulin secretion (94% over basal, P<0.05). Injection of the α2-adrenergic agonist clonidine into MPOA produced a faster, more intense and longer-lasting hyperglycemic response (69% over basal, P<0.01). In contrast to the noradrenaline effect on insulin secretion, clonidine markedly decreased plasma insulin levels, reaching a maximal suppression at 10 min (72% below basal, P<0.01). On the other hand, the β-adrenergic agonist isoproterenol only produced a small, transient increase in plasma glucose levels. When rats were pre-treated with guanethidine (10 mg/100 g, i.p.), despite reduced baseline of plasma glucose (35% smaller then control group, P<0.01) and increased plasma insulin baseline (300% higher then control group, P<0.01), they still showed a hyperglycemic response to noradrenaline injection into MPOA. We conclude that the activation of preoptic α 2-adrenoceptors induced hyperglycemia and inhibit insulin secretion, probably by activation of the sympathoadrenal system that cannot be blocked by prior administration of guanethidine.