BOSTON – October 17, 2011 – in a paper published today Diabetologia, in a team on Joslin’s Diabetes Center, led by Mary r. Loeken, PhD, has identified AMP kinase (AMPK) enzyme as a key molecular mechanisms to significantly increase the risk of neural tube defects such as spina bifida and heart defects among babies born with diabetes.
Even if a woman with diabetes–either type 1 or type 2–work vigilantly to their blood sugar levels around the time of conception, the risk of disability is still twice the general population. This finding could lead to strategies to disrupt the mechanism and reduce the chances of such birth defects that occur.
An earlier study published by the Loeken’s laboratory showed that maternal hyperglycemia (high blood sugar) causes the embryo, and oxidative stress inhibits Pax3 gene expression. Pax3 is important for the formation of the neural tube, which in the embryo is a precursor to the brain and spinal cord. Oxidative stress results when oxidized molecules called free radicals-created faster than they can be removed.
However, Loeken says, it is not yet known how the cells expressing Pax3 could feel the oxidative stress and why oxidative stress, which occurs throughout the embryo, the only damage to the structure of selective neural tube-like.
In the paper published today, the team identifies key to Loeken’s process as AMP kinase, which is activated by oxidative stress and cell nucleus signal was found to block the expression of Pax3.