{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T23:01:10Z","timestamp":1791846070282,"version":"4.3.4"},"reference-count":66,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2016,6,14]],"date-time":"2016-06-14T00:00:00Z","timestamp":1465862400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"name":"The Suncoast Cardiovascular Research and Education Foundation"},{"name":"The David and Janice Mason Fund"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Birth Defects Research"],"published-print":{"date-parts":[[2016,9]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Embryonic acute exposure to ethanol (EtOH), lithium, and homocysteine (HCy) induces cardiac defects at the time of exposure; folic acid (FA) supplementation protects normal cardiogenesis (Han et al., <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"#bdra23526-bib-0024\"\/>, <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"#bdra23526-bib-0023\"\/>; Serrano et al., <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"#bdra23526-bib-0049\"\/>). Our hypothesis is that EtOH exposure and FA protection relate to lipid and FA metabolism during mouse cardiogenesis and placentation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>On the morning of conception, pregnant C57BL\/6J mice were placed on either of two FA\u2010containing diets: a 3.3 mg health maintenance diet or a high FA diet of 10.5 mg\/kg. Mice were injected a binge level of EtOH, HCy, or saline on embryonic day (E) 6.75, targeting gastrulation. On E15.5, cardiac and umbilical blood flow were examined by ultrasound. Embryonic cardiac tissues were processed for gene expression of lipid and FA metabolism; the placenta and heart tissues for neutral lipid droplets, or for medium chain acyl\u2010dehydrogenase (MCAD) protein.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>EtOH exposure altered lipid\u2010related gene expression on E7.5 in comparison to control or FA\u2010supplemented groups and remained altered on E15.5 similarly to changes with HCy, signifying FA deficiency. In comparison to control tissues, the lipid\u2010related <jats:italic>acyl CoA dehydrogenase medium length chain<\/jats:italic> gene and its protein MCAD were altered with EtOH exposure, as were neutral lipid droplet localization in the heart and placenta.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>EtOH altered gene expression associated with lipid and folate metabolism, as well as neutral lipids, in the E15.5 abnormally functioning heart and placenta. In comparison to controls, the high FA diet protected the embryo and placenta from these effects allowing normal development. Birth Defects Research (Part A) 106:749\u2013760, 2016. \u00a9 2016 The Authors Birth Defects Research Part A: Clinical and Molecular Teratology Published by Wiley Periodicals, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/bdra.23526","type":"journal-article","created":{"date-parts":[[2016,6,14]],"date-time":"2016-06-14T11:33:05Z","timestamp":1465903985000},"page":"749-760","source":"Crossref","is-referenced-by-count":18,"title":["Acute alcohol exposure during mouse gastrulation alters lipid metabolism in placental and heart development: Folate prevention"],"prefix":"10.1002","volume":"106","author":[{"given":"Kersti K.","family":"Linask","sequence":"first","affiliation":[{"name":"Department of Pediatrics USF Morsani College of Medicine Tampa and St. Petersburg Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mingda","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Pediatrics USF Morsani College of Medicine Tampa and St. Petersburg 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