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

机译:视前内侧肾上腺素能受体调节自由运动大鼠的血糖和胰岛素血症。

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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, thebeta-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 alpha(2)-adrenoceptors induced hyperglycemia and inhibit insulin secretion, probably by activation of the sympathoadrenal system that cannot be blocked by prior administration of guanethidine.
机译:为了研究内侧视前区(MPOA)肾上腺素受体在调节血浆葡萄糖和胰岛素分泌中的作用,我们向自由运动的Wistar大鼠的MPOA中注射了40 nmol的去甲肾上腺素,可乐定或异丙肾上腺素。这些动物装有慢性颈静脉导管以进行血液采样,并将单侧脑内导管置入MPOA中。结果表明,去甲肾上腺素注射到MPOA中可使血浆葡萄糖水平和胰岛素分泌快速增加,在刺激后15分钟血浆葡萄糖水平达到峰值(基础值的25%,P <0.01),在胰岛素分泌30分钟达到峰值(94)。超过基础的百分比,P <0.05)。向MPOA中注射α2-肾上腺素能激动剂可乐定可产生更快,更强烈和更持久的高血糖反应(占基础的69%,P <0.01)。与去甲肾上腺素对胰岛素分泌的影响相反,可乐定显着降低血浆胰岛素水平,在10分钟时达到最大抑制作用(低于基础值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浆葡萄糖水平产生短暂的短暂增加。当大鼠用胍乙啶(10 mg / 100 g,腹膜内)预处理时,尽管血浆葡萄糖基线降低(比对照组小35%,P <0.01),血浆胰岛素基线升高(比对照组P高300%) <0.01),他们仍然显示出将去甲肾上腺素注射入MPOA的高血糖反应。我们得出的结论是,视前α(2)-肾上腺素受体的激活可能引起高血糖症并抑制胰岛素分泌,这可能是由于交感肾上腺系统的激活所致,而该交感肾上腺系统不能被先前的胍乙啶阻断。

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