Sullivan Kelli A, Hayes John M, Wiggin Timothy D, Backus Carey, Su Oh Sang, Lentz Stephen I, Brosius Frank, Feldman Eva L
Department of Neurology, University of Michigan, Ann Arbor, MI 48109-2200, USA.
Neurobiol Dis. 2007 Dec;28(3):276-85. doi: 10.1016/j.nbd.2007.07.022. Epub 2007 Jul 31.
Diabetic neuropathy (DN) is a debilitating complication of type 1 and type 2 diabetes. Rodent models of DN do not fully replicate the pathology observed in human patients. We examined DN in streptozotocin (STZ)-induced [B6] and spontaneous type 1 diabetes [B6Ins2(Akita)] and spontaneous type 2 diabetes [B6-db/db, BKS-db/db]. Despite persistent hyperglycemia, the STZ-treated B6 and B6Ins2(Akita) mice were resistant to the development of DN. In contrast, DN developed in both type 2 diabetes models: the B6-db/db and BKS-db/db mice. The persistence of hyperglycemia and development of DN in the B6-db/db mice required an increased fat diet while the BKS-db/db mice developed severe DN and remained hyperglycemic on standard mouse chow. Our data support the hypothesis that genetic background and diet influence the development of DN and should be considered when developing new models of DN.
糖尿病神经病变（DN）是1型和2型糖尿病的一种使人衰弱的并发症。DN的啮齿动物模型不能完全复制在人类患者中观察到的病理情况。我们研究了链脲佐菌素（STZ）诱导的[B6]1型糖尿病、自发性1型糖尿病[B6Ins2（Akita）]以及自发性2型糖尿病[B6-db/db、BKS-db/db]中的DN。尽管存在持续性高血糖，但经STZ处理的B6和B6Ins2（Akita）小鼠对DN的发生具有抗性。相比之下，两种2型糖尿病模型（B6-db/db和BKS-db/db小鼠）均发生了DN。B6-db/db小鼠中高血糖的持续存在和DN的发生需要增加高脂饮食，而BKS-db/db小鼠则发生了严重的DN，并且在标准小鼠饲料喂养下仍保持高血糖。我们的数据支持这样的假设，即遗传背景和饮食会影响DN的发生，并且在开发新的DN模型时应予以考虑。
