Kasselman Lora J, Veves Aristidis, Gibbons Christopher H, Rutkove Seward B
Division of Neuromuscular Diseases, Department of Neurology, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215, USA.
Exp Diabetes Res. 2009;2009:827943. doi: 10.1155/2009/827943. Epub 2010 Jan 14.
Diabetic polyneuropathy (DPN) and cold-induced nerve injury share several pathogenic mechanisms. This study explores whether cold exposure contributes to the development of DPN. Streptozotocin-induced diabetic rats and controls were exposed to a room temperature (23 degrees C) or cold environment (10 degrees C). H-reflex, tail and sciatic motor, and sensory nerve conduction studies were performed. Analyses of sural nerve, intraepidermal nerve fibers, and skin and nerve nitrotyrosine ELISAs were performed. Diabetic animals exposed to a cold environment had an increased H-reflex four weeks earlier than diabetic room temperature animals (P = .03). Cold-exposed diabetic animals also had greater reduction in motor conduction velocities at 20 weeks (P = .017), decreased skin nerve fiber density (P = .037), and increased skin nitrotyrosine levels (P = .047). Cold exposure appears to hasten the development of DPN in the rat STZ model of diabetes. These findings support that further study into the relationship between ambient temperature and DPN is warranted.
糖尿病性多发性神经病变（DPN）与冷诱导神经损伤具有若干共同的致病机制。本研究探讨寒冷暴露是否会促使DPN的发生发展。将链脲佐菌素诱导的糖尿病大鼠及对照大鼠暴露于室温（23摄氏度）或寒冷环境（10摄氏度）中。进行了H反射、尾部及坐骨神经运动和感觉神经传导研究。对腓肠神经、表皮内神经纤维以及皮肤和神经硝基酪氨酸酶联免疫吸附测定（ELISA）进行了分析。暴露于寒冷环境的糖尿病动物比处于室温的糖尿病动物早四周出现H反射增强（P = 0.03）。暴露于寒冷环境的糖尿病动物在20周时运动传导速度的降低也更明显（P = 0.017），皮肤神经纤维密度降低（P = 0.037），皮肤硝基酪氨酸水平升高（P = 0.047）。在大鼠糖尿病链脲佐菌素模型中，寒冷暴露似乎会加速DPN的发生发展。这些发现支持有必要进一步研究环境温度与DPN之间的关系。
