Ishii D N, Lupien S B
Department of Physiology, Colorado State University, Fort Collins 80523.
J Neurosci Res. 1995 Jan 1;40(1):138-44. doi: 10.1002/jnr.490400116.
Neuropathy is an enigmatic and debilitating complication of diabetes. A consensus as to the pathogenesis of this disorder has yet to emerge. Recently, it has been found that the insulin-like growth factors (IGFs) regulate peripheral nerve regeneration, and IGF content is reduced in various diabetic tissues. We tested herein the hypothesis that IGF administration can prevent or ameliorate the impairment of sensory nerve regeneration in streptozotocin diabetic rats. Miniosmotic pumps released small local doses of IGF-I from a catheter routed near a site of sciatic nerve crush or larger systemic doses of IGF-I or IGF-II from a distant subcutaneous site. Whether administered locally or systemically, IGFs protected against the impairment of sensory nerve regeneration. Surprisingly, this protection was obtained despite unabated hyperglycemia. Therefore, the neuropathy involving sensory nerve regeneration in diabetes can be ameliorated or prevented by IGF treatment, independently of hyperglycemia.
神经病变是糖尿病一种难以捉摸且使人衰弱的并发症。关于这种疾病的发病机制尚未达成共识。最近，人们发现胰岛素样生长因子（IGFs）可调节外周神经再生，且在各种糖尿病组织中IGF含量会降低。我们在此测试了这样一个假设，即给予IGF可以预防或改善链脲佐菌素诱导的糖尿病大鼠感觉神经再生的损伤。微型渗透泵从坐骨神经挤压部位附近的导管释放小剂量局部IGF-I，或从远处皮下部位释放大剂量全身性IGF-I或IGF-II。无论局部给药还是全身给药，IGFs都能防止感觉神经再生受损。令人惊讶的是，尽管高血糖未得到缓解，但仍获得了这种保护作用。因此，糖尿病中涉及感觉神经再生的神经病变可通过IGF治疗得到改善或预防，且与高血糖无关。
