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Rosiglitazone Linked to Less Neuropathy in Diabetic Mice

Researchers find transcription factor binding modules likely involved in diabetic neuropathy

THURSDAY, July 3 (HealthDay News) -- In a mouse model of diabetic neuropathy, rosiglitazone improved a measure of thermal latency and reduced oxidative stress in the sciatic nerve, and novel transcriptional control sequences were found in genes correlated with diabetic neuropathy, according to research published online June 26 in Endocrinology.

Timothy D. Wiggin, of the University of Michigan in Ann Arbor, and colleagues analyzed data from experiments on DBA/2J mice, divided into four groups: control, diabetic, control with rosiglitazone treatment, and diabetic with rosiglitazone treatment. Thermal latency was assessed by measuring time to withdrawal of a hind paw from a heat source.

The researchers found that the treated diabetic mice had lower thermal latency -- thus less neuropathy -- than diabetic mice, despite the same mean blood glucose. Rosiglitazone also reduced sciatic oxidative stress. The drug significantly up-regulated the genes containing SP1F_ZBPF or EGRF_EGRF modules, which likely play a role in the development of diabetic neuropathy, according to the authors.

"In conclusion, this study demonstrates that the [streptozotocin-induced diabetic DBA/2J] mouse develops and maintains diabetic neuropathy. Diabetic neuropathy is highly correlated with the oxidative stress present in the sciatic nerve, and both are reduced by rosiglitazone treatment. Using a systems biology approach, we found significant changes in gene expression induced by diabetes and rosiglitazone, and that two TF binding modules, SP1F_ZBPF and EGRF_EGRF, are likely involved. These modules constitute novel drug targets, and merit future study," Wiggin and colleagues write.

A study co-author disclosed receiving lecture fees from Merck/Schering Plough.

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