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Rosiglitazone Treatment Reduces Diabetic Neuropathy in STZ treated DBA/2J mice
Timothy D Wiggin, Matthias Kretzler, Subramaniam Pennathur, Kelli A. Sullivan,
Frank C Brosius, Eva L Feldman
Eva Feldman on 4/4/2008
Volume : Pages
149(10) : 4928 - 4937
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
University of Arizona
University of Michigan
University of Michigan
Neuropathy & Neurocognition
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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