Mouse models of diabetic neuropathy

被引：155

作者：

Sullivan, Kelli A. ^{[1
]}

Hayes, John M. ^{[1
]}

Wiggin, Timothy D. ^{[1
]}

Backus, Carey ^{[1
]}

Oh, Sang Su ^{[1
]}

Lentz, Stephen I. ^{[3
]}

Brosius, Frank, III ^{[2
]}

Feldman, Eva L. ^{[1
]}

机构：

[1] Univ Michigan, Dept Neurol, Ann Arbor, MI 48109 USA

[2] Univ Michigan, Div Nephrol, Dept Internal Med, Ann Arbor, MI 48109 USA

[3] Univ Michigan, Div Endocrinol & Metab, Dept Internal Med, Ann Arbor, MI 48109 USA

来源：

NEUROBIOLOGY OF DISEASE | 2007年 / 28卷 / 03期

关键词：

BKS; streptozotocin; B6Ins2(Akita); sciatic nerve; dorsal root ganglia; PERIPHERAL NEUROPATHY; NEUROTROPHIN TREATMENT; NITROSATIVE STRESS; ALDOSE REDUCTASE; COMPLICATIONS; APOPTOSIS; C57BL/6J; NEURONS; OBESITY; HYPERGLYCEMIA;

D O I：

10.1016/j.nbd.2007.07.022

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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. (C) 2007 Elsevier Inc. All rights reserved.

引用

页码：276 / 285

页数：10

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