Gestational diabetes mellitus (GDM) is a worldwide pregnancy complication. Gestational diabetes can significantly impact fetus development. However, the effects of high glucose on embryological development post-fertilization are yet to be researched. Danio rerio embryos are a great model for studying embryonic development. In this study, the effects on embryological (morphological and genetic) development were examined in the presence of a high-glucose environment that mimics the developing fetus in pregnant women with GDM. Fertilized zebrafish embryos were treated with normal media and high glucose for 5 days from 3 h post-fertilization (hpf) to 96 hpf, respectively, as control and experimental groups. Morphological changes are recorded with microscope images. Hatch rate and heart rate are compared between groups at set time points. RNA-Seq is performed to examine the gene changes in the experimental group. Glucose delayed the zebrafish embryo development by slowing the hatch rate by about 24 h. The brain, heart, and tail started showing smaller morphology in the glucose group compared to the control group at 24 hpf. Heart rate was faster in the glucose group compared to the control group on days 2 and 3 with a statistically significant difference. Among the zebrafish whole genome, the significantly changed genes were 556 upregulated genes and 1118 downregulated genes, respectively, in the high-glucose group. The metabolic and Wnt pathways are altered under high-glucose conditions. These conditions contribute to significant physiological differences that may provide insight into the functionality of post-embryological development.

Gestational Diabetes Mellitus (GDMs) is worldly wide pregnancy complication. Gestational Diabetes can significantly impact the fetus development. However, the effects of high glucose on embryological development post-fertilization are yet to be researched. Danio rerio embryos are great model to study the embryonic development. In this study, the effects on embryological (morphological and genetic) development were examined in the presence of a high glucose environment that mimic the developing fetus in pregnant women with GMD. Fertilized Zebrafish embryos were treated with normal media and high glucose for 5 days from 3 hours post-fertilization(hpf) to 96hpf respectively as control and experimental groups. Morphological changes are recorded with Microscope images. Hatch rate and heart rate are compared between groups in set up time points. RNA-Seq is performed to examine the gene changes in experimental group. Glucose delayed the zebrafish embryo development by slowing the hatch rate about 24 hours. The brain, heart, and tail started showing morphology smaller in the glucose group compared to the control group at 24 hpf. Heart rate is faster in the glucose group compared to the control group on day 2 and 3 with a statistically significant difference. Among zebrafish whole genome, the significantly changed genes are 556 genes up-regulated and 1118 genes down-regulated respectively in high glucose group. The metabolic and Wnt pathways are altered under high glucose condition. These conditions contribute to significant physiological differences that may provide insight on functionality post-embryological development.

Cardiovascular disease and hypertension are major global health challenges, and increasing dietary salt intake is a known contributor. Emerging evidence suggests that excessive salt exposure during pregnancy may impact fetal development, yet its effects on early embryogenesis remain poorly understood. In this study, we used zebrafish (Danio rerio) embryos as a model to investigate the developmental and molecular consequences of high-salt exposure during early vertebrate development. Embryos subjected to elevated salt levels exhibited delayed hatching, reduced heart rates, and significant alterations in gene expression profiles. Transcriptomic analysis revealed over 4000 differentially expressed genes, with key disruptions identified in calcium signaling, MAPK signaling, cardiac muscle development, and vascular smooth muscle contraction pathways. These findings indicate that early salt exposure can perturb crucial developmental processes and signaling networks, offering insights into how prenatal environmental factors may contribute to long-term cardiovascular risk.

Cardiovascular disease and hypertension are leading global health concerns. Modern fast-paced lifestyles have contributed to increased dietary salt intake, which affects not only adults but also fetal development. However, the impact of high salt exposure on embryogenesis remains underexplored. Danio rerio (zebrafish) embryos offer a powerful model for studying vertebrate development due to their transparency, rapid growth, and physiological similarity to humans. In this study, we examined the morphological and genetic effects of high salt exposure using a 2% NaCl environment to simulate conditions relevant to maternal high salt intake during pregnancy. Fertilized zebrafish embryos were exposed to either standard media (control) or 2% salt from 3 hours post-fertilization (hpf) to 96 hpf. Morphological development was documented through microscopy, and hatch and heart rates were assessed at multiple time points. RNA sequencing (RNA-Seq) was performed to identify gene expression changes associated with salt exposure. High salt treatment delayed embryonic development, with hatch rates lagging approximately 24 hours behind controls. Heart rate was significantly reduced in the salt group on days 2 and 3. Transcriptomic analysis revealed substantial changes in gene expression, with 2,133 genes upregulated and 2,190 downregulated in the salt-treated group. Pathway enrichment analysis identified disruptions in calcium signaling, MAPK signaling, cardiac muscle development, and vascular smooth muscle contraction. These findings suggest that high salt exposure during early development alters critical signaling pathways and physiological processes, providing mechanistic insights that may inform our understanding of cardiovascular risk programming during fetal development.

Caffeine exposure during pregnancy has been associated with developmental abnormalities; however, the combined effects of caffeine and glucose on embryogenesis remain unclear. In this study, zebrafish embryos were exposed to caffeine or caffeine plus glucose co-treatment from 3 hours post-fertilization to 96 hours post-fertilization to evaluate developmental, physiological, and transcriptomic changes. Morphological analyses revealed developmental abnormalities in treatment groups, including pericardial edema, abnormal body curvature, delayed tail extension, and enlarged yolk sac morphology. Significant alterations in hatch rate and heart rate were also observed following treatment exposure. RNA sequencing analysis demonstrated that caffeine induced broad transcriptomic disruption involving neuronal signaling, embryonic development, metabolism, mitochondrial activity, immune regulation, and protein turnover pathways. Compared with caffeine treatment alone, glucose co-treatment reduced the magnitude of differential gene expression and modulated developmental and metabolic signaling pathways. Alternative splicing analysis further identified widespread exon-skipping events and altered splicing patterns in genes associated with developmental and neuronal regulation. Collectively, these findings demonstrate that glucose supplementation partially reshapes caffeine-induced developmental and transcriptomic dysregulation during zebrafish embryogenesis.

Caffeine exposure during pregnancy has been associated with developmental abnormalities; however, the combined effects of caffeine and glucose on embryogenesis remain unclear. In this study, zebrafish embryos were exposed to caffeine or caffeine plus glucose co-treatment from 3 h post-fertilization to 96 h post-fertilization to evaluate developmental, physiological, and transcriptomic changes. Morphological analyses revealed developmental abnormalities in treatment groups, including pericardial edema, abnormal body curvature, delayed tail extension, and enlarged yolk sac morphology. Significant alterations in hatch rate and heart rate were also observed following treatment exposure. RNA sequencing analysis demonstrated that caffeine induced broad transcriptomic disruption involving neuronal signaling, embryonic development, metabolism, mitochondrial activity, immune regulation, and protein turnover pathways. Compared with caffeine treatment alone, caffeine plus glucose co-treatment was associated with differences in differential gene expression and developmental and metabolic signaling pathways. Alternative splicing analysis further identified widespread exon-skipping events and altered splicing patterns in genes associated with developmental and neuronal regulation. Collectively, these findings indicate that glucose co-treatment was associated with altered developmental and transcriptomic responses relative to caffeine exposure alone during zebrafish embryogenesis. Because a glucose-only treatment was not included in the present study, these findings should not be interpreted as demonstrating a definitive caffeine–glucose interaction.