{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:16:23Z","timestamp":1787015783766,"version":"build-2736575974"},"reference-count":56,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2020,12,10]],"date-time":"2020-12-10T00:00:00Z","timestamp":1607558400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["nyaspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Annals of the New York Academy of Sciences"],"published-print":{"date-parts":[[2021,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Many studies have shown that vitamin D (VD) deficiency may be a risk factor for neurodevelopmental disorders, such as autism spectrum disorders (ASDs) and schizophrenia, although causative mechanisms remain unknown. In this study, we investigated the potential role and effect of VD on maternal diabetes induced autism\u2010related phenotypes. The\n                    <jats:italic>in vitro<\/jats:italic>\n                    study found that enhancing genomic VD signaling by overexpressing the VD receptor (VDR) in human neural progenitor cells ACS\u20105003 protects against hyperglycemia\u2010induced oxidative stress and inflammation by activating Nrf2 and its target genes, including\n                    <jats:italic>SOD2<\/jats:italic>\n                    and\n                    <jats:italic>HMOX1<\/jats:italic>\n                    , and accordingly, VDR gene knockdown worsens the problem. In the two\n                    <jats:italic>in vivo<\/jats:italic>\n                    models we explored, maternal diabetes was used to establish an animal model of relevance to ASD, and mice lacking 25\u2010hydroxyvitamin D 1\u2010alpha\u2010hydroxylase (the rate\u2010limiting enzyme in the synthesis of 1,25(OH)2D3) were used to develop a model of VD deficiency (VDD). We show that although prenatal VDD itself does not produce ASD\u2010relevant phenotypes, it significantly potentiates maternal diabetes induced epigenetic modifications and autism\u2010related phenotypes. Postnatal manipulation of VD has no effect on maternal diabetes induced autism\u2010related phenotypes. We conclude that VDD potentiates maternal diabetes induced autism\u2010related phenotypes in offspring by epigenetic mechanisms. This study adds to other preclinical studies linking prenatal VDD with a neurodevelopmental disorder.\n                  <\/jats:p>","DOI":"10.1111\/nyas.14535","type":"journal-article","created":{"date-parts":[[2020,12,11]],"date-time":"2020-12-11T01:45:58Z","timestamp":1607651158000},"page":"74-88","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["Vitamin D deficiency worsens maternal diabetes induced neurodevelopmental disorder by potentiating hyperglycemia\u2010mediated epigenetic changes"],"prefix":"10.1111","volume":"1491","author":[{"given":"Yujie","family":"Liang","sequence":"first","affiliation":[{"name":"Department of Child Psychiatry Kangning Hospital of Shenzhen  Shenzhen P.R. 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China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saijun","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Foshan University Foshan Maternity and Child Health Care Hospital  Foshan P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ling","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Child Psychiatry Kangning Hospital of Shenzhen  Shenzhen P.R. 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