Fujiwara T, Nagai K, Takagi S, Nakagawa H
Division of Protein Metabolism, Osaka University.
Am J Physiol. 1988 Apr;254(4 Pt 1):E468-75. doi: 10.1152/ajpendo.1988.254.4.E468.
Electrical stimulation of the lateral part of the dorsal parabrachial nucleus (PBD) induces hyperglycemia by enhancing glucagon secretion and suppressing insulin secretion in rats. The mechanism of this effect in the light period was examined by use of blockers of the autonomic nervous system. Hexamethonium, a ganglion blocker, and propranolol, a beta-adrenergic blocker, markedly inhibited the hyperglycemic response to stimulation of the lateral part of the PBD (LPBD). In contrast, phenoxybenzamine, an alpha-adrenergic blocker, and atropine methylnitrate, a muscarinic blocker, had no effect. Because previous studies showed that bilateral lesions of the suprachiasmatic nucleus (SCN) eliminated hyperglycemia induced by intracranial injection of 2-deoxy-D-glucose and that blinding largely suppressed the hyperglycemia, the effects of these two treatments on hyperglycemia induced by electrical stimulation of the LPBD were examined. SCN lesions abolished the hyperglycemic response but did not affect the hyperglucagonemic response. Results 4 wk after orbital enucleation were similar to those after SCN lesions. These findings suggest that the SCN and a beta-adrenergic mechanism are involved in the hyperglycemic response to LPBD stimulation.
电刺激大鼠臂旁背核外侧部（PBD）可通过增强胰高血糖素分泌和抑制胰岛素分泌诱导高血糖。利用自主神经系统阻滞剂研究了光照期这种效应的机制。神经节阻滞剂六甲铵和β-肾上腺素能阻滞剂普萘洛尔显著抑制了对PBD外侧部（LPBD）刺激的高血糖反应。相比之下，α-肾上腺素能阻滞剂酚苄明和毒蕈碱阻滞剂甲基硝酸阿托品则没有效果。因为先前的研究表明，视交叉上核（SCN）双侧损伤消除了颅内注射2-脱氧-D-葡萄糖诱导的高血糖，并且致盲在很大程度上抑制了高血糖，所以研究了这两种处理对电刺激LPBD诱导的高血糖的影响。SCN损伤消除了高血糖反应，但不影响高胰高血糖素反应。眼球摘除术后4周的结果与SCN损伤后的结果相似。这些发现表明，SCN和β-肾上腺素能机制参与了对LPBD刺激的高血糖反应。
