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Publication

Rosiglitazone Treatment Reduces Diabetic Neuropathy in STZ treated DBA/2J mice

Authors Timothy D Wiggin, Matthias Kretzler, Subramaniam Pennathur, Kelli A. Sullivan, Frank C Brosius, Eva L Feldman Submitted By Eva Feldman on 4/4/2008 Status Published Journal Endocrinology Year 2008 Date Published 10/1/2008 Volume : Pages 149(10) : 4928 - 4937 PubMed Reference 18583417 Abstract Diabetic Neuropathy (DN) is a common complication of diabetes. Currently, there is no drug treatment to prevent or slow the development of DN. Rosiglitazone (Rosi) is a potent insulin sensitizer and may also slow the development of DN by a mechanism independent of its effect on hyperglycemia. A two by two design was used to test the effect of Rosi treatment on the development of DN. Streptozotocin-induced diabetic DBA/2J mice were treated with Rosi. DN and oxidative stress were quantified, and gene expression was profiled using the Affymetrix Mouse Genome 430 2.0 microarray platform. An informatics approach identified key regulatory elements activated by Rosi. Diabetic DBA/2J mice developed severe hyperglycemia, DN and elevated oxidative stress. Rosi treatment did not affect hyperglycemia but did reduce oxidative stress and prevented development of thermal hypoalgesia. Two novel transcription factor binding modules were identified that may control genes correlated to changes in DN following Rosi treatment: SP1F_ZBPF and EGRF_EGRF. Rosi treatment reduced oxidative stress and DN independent of its insulin sensitizing effects. Gene expression profiling identified two novel targets activated by Rosi treatment. These targets may be useful in designing drugs with the same efficacy as Rosi in treating DN but with fewer undesirable effects.

Investigators with authorship
Name Institution Frank Brosius University of Arizona Eva Feldman University of Michigan Matthias Kretzler University of Michigan

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