Nagai K, Sekitani M, Otani K, Nakagawa H
Institute for Protein Research, Osaka University, Suita, Japan.
Life Sci. 1988;43(20):1575-82. doi: 10.1016/0024-3205(88)90528-0.
Studies were made on whether hereditary microphthalmic rats (1), which are congenitally blind, showed a hyperglycemic response to intracerebroventricular injection of 2-deoxy-D-glucose (2DG) in their subjective light period. In contrast to previous findings in normal rats in which 2DG injection caused light-cycle dependent hyperglycemia (2) and bilateral lesion of the suprachiasmatic nucleus (SCN) completely abolished this hyperglycemia (3), 2DG injection caused no and only slight hyperglycemia in male and female rats with hereditary microphthalmia, respectively. Gross and histological examinations indicated that these rats had no optic nerve or retinohypothalamic tract and that their SCN had an abnormal structure. Locomotive activity recordings showed that all the blind rats had a free-running circadian activity rhythm. These findings suggest that the projection sites of the retinohypothalamic tract to the SCN are involved in the mechanism of the hyperglycemic response to 2DG, but that neural cells, which may be responsible for the generation of circadian rhythms, are not. We have reported that when adult rats were blinded by orbital enucleation, their hyperglycemic response to 2DG was suppressed temporarily 3-5 weeks after the operation, but that their plasma insulin level was basically higher and increased further after 2DG injection during this period (4). In congenitally blind rats, however, the basal plasma insulin level was not higher and the level did not change after 2DG treatment. This difference is discussed from the view point of the role of the premature SCN in regulation of the plasma insulin concentration.
对遗传性小眼大鼠（1）进行了研究，这些大鼠先天性失明，研究其在主观光照期对脑室内注射2-脱氧-D-葡萄糖（2DG）是否表现出高血糖反应。与之前在正常大鼠中的研究结果相反，在正常大鼠中注射2DG会导致光周期依赖性高血糖（2），而视交叉上核（SCN）的双侧损伤会完全消除这种高血糖（3），注射2DG分别在患有遗传性小眼症的雄性和雌性大鼠中未引起和仅引起轻微的高血糖。大体和组织学检查表明，这些大鼠没有视神经或视网膜下丘脑束，并且它们的SCN结构异常。运动活动记录显示，所有失明大鼠都有自由运行的昼夜活动节律。这些发现表明，视网膜下丘脑束投射到SCN的部位参与了对2DG高血糖反应的机制，但可能负责昼夜节律产生的神经细胞则没有参与。我们曾报道，当成年大鼠通过眼眶摘除术致盲后，它们对2DG的高血糖反应在术后3-5周暂时受到抑制，但在此期间它们的血浆胰岛素水平基本较高，并且在注射2DG后进一步升高（4）。然而，在先天性失明的大鼠中，基础血浆胰岛素水平并不高，并且在2DG处理后水平没有变化。从过早的SCN在调节血浆胰岛素浓度中的作用的角度讨论了这种差异。
