Mouse models of diabetic neuropathy

Kelli A. Sullivan; John M. Hayes; Timothy D. Wiggin; Carey Backus; Sang Su Oh; Stephen I. Lentz; Frank Brosius, III; Eva L. Feldman

Neurobiology of Disease (Dec 2007)

Mouse models of diabetic neuropathy

Kelli A. Sullivan,
John M. Hayes,
Timothy D. Wiggin,
Carey Backus,
Sang Su Oh,
Stephen I. Lentz,
Frank Brosius, III,
Eva L. Feldman

Affiliations

Kelli A. Sullivan: Department of Neurology, University of Michigan, USA
John M. Hayes: Department of Neurology, University of Michigan, USA
Timothy D. Wiggin: Department of Neurology, University of Michigan, USA
Carey Backus: Department of Neurology, University of Michigan, USA
Sang Su Oh: Department of Neurology, University of Michigan, USA
Stephen I. Lentz: Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Michigan, Ann Arbor, MI, USA
Frank Brosius, III: Department of Internal Medicine, Division of Nephrology, University of Michigan, USA
Eva L. Feldman: Department of Neurology, University of Michigan, USA; Corresponding author. University of Michigan, Department of Neurology, 5017 Basic Science Research Building (BSRB), 109 Zina Pitcher Road, Ann Arbor, MI 48109-2200, USA. Fax: +1 734 763 7275.

Journal volume & issue: Vol. 28, no. 3
pp. 276 – 285

Abstract

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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 [B6Ins2Akita] and spontaneous type 2 diabetes [B6-db/db, BKS-db/db]. Despite persistent hyperglycemia, the STZ-treated B6 and B6Ins2Akita 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.

Published in Neurobiology of Disease

ISSN: 0969-9961 (Print); 1095-953X (Online)
Publisher: Elsevier
Country of publisher: United States
LCC subjects: Medicine: Internal medicine: Neurosciences. Biological psychiatry. Neuropsychiatry
Website: https://www.journals.elsevier.com/neurobiology-of-disease

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