Glucose as a Teratogen Affecting Cranial Neural Crest Migration in the Developing Chick Embryo

Overview

Objectives/Goals Since infants of diabetic mothers are five times as likely as the normal population to be born with a birth defect, this project aims to determine if glucose itself plays a role in these malformations. If glucose does play a role, the goal is to examine how glucose is able to bring about these defects. Methods/Materials Fertilized chick eggs were incubated until proper stages were reached (stages 4, 7, or 8; Hamburger and Hamilton, 1955). Over 350 embryos were used in each control/experimental stage. Embryos were cultured either in vitro (stage 4) or in vivo (stages 7 and 8) and then subjected to varying amounts of glucose or sucrose (the control) through use of a Picospritzer. For studies involving uPA inhibition, a 1mM solution of Amiloride was added. Cultures were incubated for a further 24 hours to 7 days and then fixed in 4% Paraformaldehyde. Immunohistochemistry was performed on stage 4 embryos to label for the gene Hnk-1. Older embryos were examined visually using a dissection microscope. Results Embryos subjected to a 1.08M solution of glucose showed cardiovascular and craniofacial defects. 57% of embryos developing in 0.36M glucose showed some sort of craniofacial defects in contrast to the 8% in the control. A dominant craniofacial defect shown was open neural tubes. Inhibition of uPA showed dark labeling down the midline of the embryo suggesting that neural crest cells stayed premigratory. For stage 4 embryos, only 4% showed neural tube closure in contrast to the 100% closure rate of control embryos. Conclusions/Discussion Cardiovascular defects are significant in that these defects are seen in other teratogens. Also, results show that as glucose concentrations increase, so does the likelihood that an embryo will develop some sort of a defect. I had hypothesized that glucose is able to inhibit the migratory abilities of neural crest which brings about the defects and the results indicate that this hypothesis is valid. Inhibiting uPA allowed me to examine effects of neural crest inhibition and results suggest that embryos subjected to glucose do indeed have non-migratory crest. It is widely known that diabetics have a higher chance of giving birth to a defective child, but glucose (at higher than normal concentrations) has never been classified as a teratogen. This study initiates more studies hopefully leading to glucose being added to the list of known teratogens.

Competition history

• CSEF 2003 Pharmacology/ Toxicology · Entry S1416

Resources

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