Publication Date

Spring 3-23-2026

Presentation Length

Poster/Gallery presentation

College

College of Sciences & Mathematics

Department

Psychological Sciences and Neurosciences, Department of

Student Level

Undergraduate

Faculty Mentor

Dr. Jinhee Park

Metadata/Fulltext

Metadata ONLY

Presentation Type

Poster

Summary

Prenatal diabetes is a critical medical condition that extensively affects neonatal patients and their families. Numerous previous studies have suggested impairments in vascular development, size, and diversification; however, the molecular and gene regulatory mechanisms underlying these effects remain poorly understood. Understanding these mechanisms is essential for identifying potential therapeutic targets and improving treatment strategies. This study combined experimental zebrafish phenotypic analysis with re-analysis of publicly available RNA-seq data to investigate the effects of elevated glucose on embryonic vascular development. Zebrafish (Danio rerio) embryos were exposed to increasing glucose concentrations (1–3%) during early developmental stages. High glucose exposure showed a trend toward decreased heart rate, along with reduced length and intensity of blood vessels in both head and tail regions, particularly at 3% glucose. At higher concentrations, embryos exhibited severe morphological defects and loss of viability. To further investigate the underlying molecular mechanisms, RNA-seq data were re-analyzed to identify gene expression changes associated with prenatal hyperglycemia. Differential expression analysis using edgeR identified 478 differentially expressed genes (DEGs) (p < 0.05), including 70 upregulated and 408 downregulated genes. Pathway analysis and GSEA revealed enrichment of genes involved in vascular development, cellular adhesion, and lipid metabolism, suggesting disruption of processes required for normal vessel formation. Together, these findings suggest that elevated glucose levels may impair both the morphological and molecular aspects of vascular development. This integrated approach provides insight into potential pathways and gene targets that could be explored in future studies investigating therapeutic strategies for prenatal diabetes.

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