Exploring hyperglycemia's impact on embryonic development: Insights from the chicken embryo model.

Abstract

Hyperglycemia during pregnancy is a growing health concern due to its association with congenital anomalies. While rodent models have been used to study this condition, their variability and inability to control the embryonic microenvironment is a limitation. Having this in mind, this study explores the chicken embryo (Gallus gallus) as an alternative model for studying the effects of hyperglycemia on early embryonic development. For that purpose, fertilized chicken eggs were exposed to glucose (0.2 and 0.4 mmol) from embryonic day 1 (E1) onwards. On embryonic day 5 (E5), glucose levels, developmental outcomes, and molecular alterations were assessed in the embryos. Hyperglycemia led to a significant increase in glucose concentration in both the surrounding environment and the embryo's bloodstream. High glucose levels caused developmental toxicity, namely increased mortality and severe abnormalities such as defects in the optic organ, brain, heart, and neural tube. Molecular analysis demonstrated an increase in igf2 and a decrease in glut1 expression in the liver, which may point to a potential protective response to high glucose levels despite the absence of insulin. Superoxide Dismutase activity was reduced suggesting an oxidative stress response. In conclusion, this study retrieves the chicken embryo model for researching hyperglycemia's effect on embryonic development, providing insights into potential molecular mechanisms and highlighting its relevance for future teratogenic research.