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Transl. Med."],"published-print":{"date-parts":[[2026,3,4]]},"abstract":"<jats:p>\n                    Gestational diabetes mellitus (GDM) can increase the risk for diabetes in offspring, but the mechanisms underlying the effects of intrauterine hyperglycemia (IHG) on the fetus remain unknown. Here, we show that IHG down-regulated DNA demethylases TET2\/3 in fetal pancreatic islets, increased DNA methylation of \u03b3-aminobutyric acid (GABA) synthesis gene\n                    <jats:italic toggle=\"yes\">Gad1<\/jats:italic>\n                    , suppressed\n                    <jats:italic toggle=\"yes\">Gad1<\/jats:italic>\n                    expression, and elevated somatostatin (SST) protein in the pancreas in mice. Pancreas-specific double knockout (DKO) of\n                    <jats:italic toggle=\"yes\">Tet2\/3<\/jats:italic>\n                    recapitulates the IHG effects, causing\n                    <jats:italic toggle=\"yes\">Gad1<\/jats:italic>\n                    hypermethylation and expression down-regulation, alongside impaired insulin secretion and glucose tolerance. Metabolomic analysis revealed that IHG and\n                    <jats:italic toggle=\"yes\">Tet2\/3<\/jats:italic>\n                    DKO reduced pancreatic GABA content. Gestational dietary GABA supplementation improved metabolic defects in both IHG and\n                    <jats:italic toggle=\"yes\">Tet2\/3<\/jats:italic>\n                    DKO models. scRNA-seq analysis of pancreatic islets showed that IHG or\n                    <jats:italic toggle=\"yes\">Tet2\/3<\/jats:italic>\n                    DKO down-regulated the \u03b2 cell signature, whereas up-regulating \u03b4 cell\u2013related genes, particularly\n                    <jats:italic toggle=\"yes\">Sst<\/jats:italic>\n                    , led to the emergence of an\n                    <jats:italic toggle=\"yes\">Ins2\/Sst<\/jats:italic>\n                    double-positive cell population. \u03b2 cell\u2013specific deletion of\n                    <jats:italic toggle=\"yes\">Sst<\/jats:italic>\n                    rescued IHG-induced metabolic defects. In humans, GDM was associated with reduced GABA content in the umbilical arterial blood. These results uncover an epigenetically controlled pancreatic GABA-SST signaling pathway that may contribute to the GDM-induced increase in offspring diabetes risk and identify dietary GABA supplementation as a potential interventional strategy.\n                  <\/jats:p>","DOI":"10.1126\/scitranslmed.adx8909","type":"journal-article","created":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T18:58:28Z","timestamp":1772650708000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":3,"title":["Epigenetically regulated pancreatic GABA-somatostatin signaling underlies gestational diabetes\u2013induced glucose intolerance in offspring"],"prefix":"10.1126","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7995-7726","authenticated-orcid":true,"given":"Hong","family":"Zhu","sequence":"first","affiliation":[{"name":"Obstetrics and Gynecology Hospital, Institute of Reproduction and Development, Fudan University, 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