ArticleCell communication and signaling : CCS2024
Dexamethasone exposure during pregnancy triggers metabolic syndrome in offspring via epigenetic alteration of IGF1.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- Single Antenatal Exposure to Ciclesonide Reduces Long-Term Cardiac Structural and Functional Alterations Compared to Currently Approved Synthetic Corticosteroids.Research square · 2026Article
- Comparable organs weights and histopathological changes after administration of dexamethasone during pregnancy in rats.Open veterinary journal · 2026Article
- Serpina3c protects against metabolic dysfunction-associated steatotic liver disease in offspring induced by prenatal prednisone exposure.Signal transduction and targeted therapy · 2026Article
- Perinatal HPA axis regulation and offspring neuropsychiatric development: mechanisms, developmental trajectories, and clinical implications.Frontiers in endocrinology · 2026Review
- Developmental regulation of fetal mitochondrial respiratory function towards term: the role of glucocorticoid and thyroid hormones.The Journal of endocrinology · 2025Review
- Dexamethasone induces transgenerational inheritance of fetal-derived glomerulosclerosis phenotype in offspring through GR/DNMT3a mediated alterations of the lncRNA-Meg3/Notch signaling pathway.Cell communication and signaling : CCS · 2025Article
- Maternal high-salt intake induces sex-specific liver injury in offspring: integrative transcriptomic and therapeutic investigation.Frontiers in nutrition · 2025Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPrevious research has reported that prenatal exposure to dexamethasone (PDE) results in organ dysplasia and increased disease susceptibility in offspring. This study aimed to investigate the epigenetic mechanism of metabolic syndrome induced by PDE in offspring.
methodsPregnant Wistar rats were administered dexamethasone, and their offspring's serum and liver tissues were analyzed. The hepatocyte differentiation model was established to unveil the molecular mechanism. Neonatal cord blood samples were collected to validate the phenomenon and mechanism.
resultsThe findings demonstrated that PDE leads to insulin resistance and typical metabolic syndrome traits in adult offspring rats, which originated from fetal liver dysplasia. Additionally, PDE reduced serum corticosterone level and inhibited hepatic insulin-like growth factor 1 (IGF1) signaling in fetal rats. It further revealed that liver dysplasia and functional impairment induced by PDE persist after birth, driven by the continuous downregulation of serum corticosterone and hepatic IGF1 signaling. Both in vitro and in vivo experiments confirmed that low endogenous corticosterone reduces the histone 3 lysine 9 acetylation (H3K27ac) level of IGF1 and its expression by blocking glucocorticoid receptor α, special protein 1, and P300 into the nucleus, resulting in hepatocyte differentiation inhibition and liver dysplasia. Intriguingly, neonatal cord blood samples validated the link between reduced liver function in neonates induced by PDE and decreased serum cortisol and IGF1 levels.
conclusionsThis study demonstrated that low endogenous glucocorticoid level under PDE lead to liver dysplasia by downregulating the H3K27ac level of IGF1 and its expression, ultimately contributing to metabolic syndrome in adult offspring.
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