Fóscolo Rodrigo Bastos, de Castro Mauricio Gustavo Bravim, Marubayashi Umeko, dos Reis Adelina Martha, Coimbra Cândido Celso
Department of Physiology and Biophysics, Institute of Biological Science, Federal University of Minas Gerais, Av. Antônio Carlos 6627, 31270-901 Belo Horizonte, MG, Brazil.
Brain Res. 2003 Sep 19;985(1):56-64. doi: 10.1016/s0006-8993(03)03158-5.
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 alpha2-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 beta-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 alpha2-adrenoceptors induced hyperglycemia and inhibit insulin secretion, probably by activation of the sympathoadrenal system that cannot be blocked by prior administration of guanethidine.
为了研究内侧视前区（MPOA）肾上腺素能受体在调节血糖和胰岛素分泌中的作用，我们向自由活动的Wistar大鼠的MPOA内注射了40 nmol去甲肾上腺素、可乐定或异丙肾上腺素。这些动物安装有用于采血的慢性颈静脉导管，并在MPOA内放置了单侧脑内插管。结果显示，向MPOA内注射去甲肾上腺素可使血糖水平和胰岛素分泌迅速升高，血糖在刺激后15分钟达到峰值（比基础值高25%，P<0.01），胰岛素分泌在30分钟达到峰值（比基础值高94%，P<0.05）。向MPOA内注射α2肾上腺素能激动剂可乐定可产生更快、更强且更持久的高血糖反应（比基础值高69%，P<0.01）。与去甲肾上腺素对胰岛素分泌的作用相反，可乐定显著降低血浆胰岛素水平，在10分钟时达到最大抑制（比基础值低72%，P<0.01）。另一方面，β肾上腺素能激动剂异丙肾上腺素仅使血糖水平产生轻微的短暂升高。当大鼠预先用胍乙啶（10 mg/100 g，腹腔注射）处理时，尽管血糖基线降低（比对照组小35%，P<0.01）且血浆胰岛素基线升高（比对照组高300%，P<0.01），但它们对向MPOA内注射去甲肾上腺素仍表现出高血糖反应。我们得出结论，视前区α2肾上腺素能受体的激活诱导高血糖并抑制胰岛素分泌，可能是通过激活交感肾上腺系统，而预先给予胍乙啶并不能阻断这种作用。
