Ishikawa T, Naito Y, Taniguchi K
Department of Veterinary Internal Medicine, Faculty of Agriculture, Iwate University, Japan.
Diabetologia. 1997 Feb;40(2):173-8. doi: 10.1007/s001250050659.
The mechanism of hearing impairment due to diabetes mellitus was examined in relation to changes in the level of the immunoreaction for the protein gene product 9.5 in the cochlea of spontaneously diabetic WBN/Kob rats. At 7 months (33 weeks) of age, when half of the males of this strain manifest diabetes, male WBN/Kob rats were divided into two groups as follows: one group consisted of prediabetic animals showing slightly decreased tolerance to glucose with a normal plasma concentration of glucose, normal urinary excretion of glucose, and functional hearing impairment (assessed in terms of elevation of hearing threshold). The second group consisted of diabetic animals with glucose intolerance, high plasma glucose level, polyuria, urinary glucose excretion, and more apparent elevation of hearing threshold. According to morphometric analysis of the spiral ganglion, the number of ganglion cells was significantly smaller in both the prediabetic and the diabetic animals than in the age-matched control Wistar rats. The staining intensity for protein gene product 9.5 was increased in some spiral ganglion cells of diabetic animals, but decreased in others according to quantitative immunohistochemical analysis. On the other hand, the immunoreactivity for protein gene product 9.5 was similar in the prediabetic animals to that in the control Wistar rats. These results suggest that numerical and immunohistochemical changes in the spiral ganglion cells reflect the onset and degree of the diabetic hearing impairment.
研究了自发性糖尿病WBN/Kob大鼠耳蜗中蛋白质基因产物9.5免疫反应水平的变化与糖尿病所致听力障碍机制之间的关系。在该品系雄性大鼠7个月（33周）龄时，即半数雄性大鼠出现糖尿病时，将雄性WBN/Kob大鼠分为以下两组：一组为糖尿病前期动物，葡萄糖耐量略有下降，血糖浓度正常，尿糖排泄正常，但存在功能性听力障碍（根据听力阈值升高进行评估）。第二组为糖尿病动物，存在葡萄糖不耐受、高血糖、多尿、尿糖排泄，且听力阈值升高更为明显。根据螺旋神经节的形态计量学分析，糖尿病前期和糖尿病动物的神经节细胞数量均显著少于年龄匹配的对照Wistar大鼠。定量免疫组织化学分析显示，糖尿病动物的一些螺旋神经节细胞中蛋白质基因产物9.5的染色强度增加，但另一些细胞中则降低。另一方面，糖尿病前期动物中蛋白质基因产物9.5的免疫反应性与对照Wistar大鼠相似。这些结果表明，螺旋神经节细胞的数量和免疫组织化学变化反映了糖尿病性听力障碍的发生和程度。
