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Gene Causing Birth Defects in Babies Born to Diabetic Mothers Identified
A team at Joslin Diabetes Center, headed by Mary R. Loeken, PhD, say that the enzyme AMP kinase (AMPK) could lead to strategies to interfere with the mechanism and reduce the chances of such birth defects occurring.
Even if women with diabetes-either type 1 or type 2 -- work vigilantly to control their blood sugar levels around the time of conception, the risk of a defect is still twice that of the general population.
Previous studies published by Loeken's lab showed that maternal hyperglycemia (high blood sugar) causes oxidative stress in the embryo, and inhibits expression of the Pax3 gene. Pax3 is essential to the formation of the neural tube, which in the embryo is the precursor to the brain and spinal cord.
However, Loeken said, it was not known how the cells that express Pax3 could sense the oxidative stress and why oxidative stress, which occurs throughout the embryo, only damages selective structures such as the neural tube.
In their new study, Loeken's team identified the key to the process as AMP kinase, which is activated by oxidative stress and was found to signal the cell nucleus to block the expression of Pax3.
"The stimulation of a metabolism-sensing enzyme that can regulate specific genes explains how oxidative stress, which is generated throughout the embryo during maternal hyperglycemia, causes malformation of specific embryo structures," Loeken said.
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More News on: Achondroplasia, DNA Finger Printing, Birth Defect - Genetic, Birth Defects - Introduction, Drug-Induced Birth Defects, Environmental Birth Defects, Birth defects - Infections, Multifactorial Birth Defects, Birth Defect - Structural Defects, Diabetes - Self-Monitoring of Blood Glucose (SMBG)
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