Journal
NEUROBIOLOGY OF DISEASE
Volume 28, Issue 3, Pages 276-285Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2007.07.022
Keywords
BKS; streptozotocin; B6Ins2(Akita); sciatic nerve; dorsal root ganglia
Categories
Funding
- NIDA NIH HHS [U54-DA021519] Funding Source: Medline
- NIDDK NIH HHS [P60 DK020572, P30 DK092926, P60 DK020572-30, 5P60 DK20572, U01 DK060994, U01 DK060994-05, DK60994] Funding Source: Medline
- NINDS NIH HHS [R01 NS038849, R01 NS038849-06, NS38849] Funding Source: Medline
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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.
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