ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2025
Transcriptome Sequencing Identifies PCK1 and IRS4 as Key Regulators of Gestational Diabetes Mellitus in Placenta: A Pilot Study.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The Placenta in Gestational Diabetes: An Integrated Review on Metabolic Pathways, Genetic, Epigenetic and Ultrasound Biomarkers for Clinical Perspectives.International journal of molecular sciences · 2026Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aim: To identify key molecular regulators of GDM in placental tissues using transcriptome sequencing. Methods: This study employed transcriptome sequencing to investigate placental tissue from GDM patients (n=7) and healthy controls (n=6), aiming to identify key molecular regulators and pathways underlying GDM pathogenesis. Results: We identified 505 differentially expressed genes (DEGs), including 216 upregulated and 289 downregulated genes. Notably, PCK1 (phosphoenolpyruvate carboxykinase 1) and IRS4 (insulin receptor substrate 4) emerged as critical regulators. Quantitative real time PCR validation confirmed significant downregulation of PCK1 and upregulation of IRS4 in GDM placentas. Functional enrichment analysis revealed that PCK1 is associated with the CLINK/HLA-G/INAVA/KLRC2/PCK1/RBP4/SLAMF6 pathway, which was suppressed in GDM, while IRS4 correlated with the dysregulated AGRP/IRS4/RXRG axis. Conclusion: These findings highlight the roles of placental PCK1 and IRS4 in GDM. Further mechanistic studies, including protein-level validation and animal models, are warranted to explore these pathways as potential diagnostic or therapeutic targets for GDM.
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