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Joslin study finds clue to birth defects in babies of mothers with diabetes
Date:10/16/2011

igator in Joslin's Section on Islet Cell and Regenerative Biology.

Trying to keep the mother's blood glucose levels under control is currently the only way to do that, she noted. "That's the best we can do right now," she said. But armed with the findings of this study, she noted, other researchers may be able to come up with drugs or other strategies to inhibit AMPK activity,

Dr. Loeken added, however, that formulating a strategy could be tricky because it is not known if interfering with AMPK activity -- while a good thing in preventing neural tube birth defects -- might also have negative effects on the embryo.

In their study Loeken and her group, including Yichao Wu, Marta Viana, and Shoba Thirumangalathu, used mice and cell lines to test their hypothesis that AMPK might be stimulated in the embryo and that stimulation of AMPK was responsible for blocking Pax3 expression and causing neural tube defects in response to high glucose.

"We found in this study that AMPK is stimulated in embryo by both high glucose and oxidative stress," Loeken said.

The study used interventions including a drug that activates AMPK and another that blocks it. The paper showed that a drug that increased AMPK activity mimics the effects of oxidative stress to inhibit expression of Pax3, thus inducing neural tube defects.


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Contact: Jeffrey Bright
jeffrey.bright@joslin.harvard.edu
Joslin Diabetes Center
Source:Eurekalert  

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