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TET-dependent signaling of β-cell underlies intrauterine hyperglycemia-induced glucose intolerance in offspring [scRNA-seq]

GSE288095 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2025/12/31 Platform GPL24247
Summary
Epidemiologically, gestational diabetes mellitus (GDM) increases offspring’s diabetes risk. Intrauterine hyperglycemia (IHG) is a typical characteristic of GDM, impairing offspring’s glucose tolerance and insulin secretion, but the underlying mechanisms remain unclear. Here, we found IHG downregulates DNA demethylases Tet2/3 in fetal pancreatic islets. Pancreas-specific Tet2/3 double knockout (DKO) recapitulates the IHG effects. scRNA-seq analysis shows IHG or DKO downregulates β-cell signature while upregulating δ-cell signature.
Published in
Epigenetically regulated pancreatic GABA-somatostatin signaling underlies gestational diabetes-induced glucose intolerance in offspring
Zhu H, Luo S, Liu C et al. · Science translational medicine 2026 · PMID 41779871 · doi:10.1126/scitranslmed.adx8909
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Also filed as BioProject PRJNA1216183 and SRA study SRP560608. Searching any of these in the dataset finder brings you back here.

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