{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T12:59:40Z","timestamp":1775048380242,"version":"3.50.1"},"reference-count":66,"publisher":"MDPI AG","issue":"5","license":[{"start":{"date-parts":[[2022,3,5]],"date-time":"2022-03-05T00:00:00Z","timestamp":1646438400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000027","name":"National Institute on Alcohol Abuse and Alcoholism","doi-asserted-by":"publisher","award":["K99 AA028291"],"award-info":[{"award-number":["K99 AA028291"]}],"id":[{"id":"10.13039\/100000027","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000027","name":"National Institute on Alcohol Abuse and Alcoholism","doi-asserted-by":"publisher","award":["R01 AA11085"],"award-info":[{"award-number":["R01 AA11085"]}],"id":[{"id":"10.13039\/100000027","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000027","name":"National Institute on Alcohol Abuse and Alcoholism","doi-asserted-by":"publisher","award":["R01 AA22999"],"award-info":[{"award-number":["R01 AA22999"]}],"id":[{"id":"10.13039\/100000027","id-type":"DOI","asserted-by":"publisher"}]},{"name":"UNC Nutrition Research Institute","award":["Internal Funding"],"award-info":[{"award-number":["Internal Funding"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nutrients"],"abstract":"<jats:p>Prenatal alcohol exposure (PAE) causes fetal growth restrictions. A major driver of fetal growth deficits is maternal metabolic disruption; this is under-investigated following PAE. Untargeted metabolomics on the dam and fetus exposed to alcohol (ALC) revealed that the hepatic metabolome of ALC and control (CON) dams were distinct, whereas that of ALC and CON fetuses were similar. Alcohol reduced maternal hepatic glucose content and enriched essential amino acid (AA) catabolites, N-acetylated AA products, urea content, and free fatty acids. These alterations suggest an attempt to minimize the glucose gap by increasing gluconeogenesis using AA and glycerol. In contrast, ALC fetuses had unchanged glucose and AA levels, suggesting an adequate draw of maternal nutrients, despite intensified stress on ALC dams. Maternal metabolites including glycolytic intermediates, AA catabolites, urea, and one-carbon-related metabolites correlated with fetal liver and brain weights, whereas lipid metabolites correlated with fetal body weight, indicating they may be drivers of fetal weight outcomes. Together, these data suggest that ALC alters maternal hepatic metabolic activity to limit glucose availability, thereby switching to alternate energy sources to meet the high-energy demands of pregnancy. Their correlation with fetal phenotypic outcomes indicates the influence of maternal metabolism on fetal growth and development.<\/jats:p>","DOI":"10.3390\/nu14051096","type":"journal-article","created":{"date-parts":[[2022,3,6]],"date-time":"2022-03-06T20:40:02Z","timestamp":1646599202000},"page":"1096","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Untargeted Metabolome Analysis Reveals Reductions in Maternal Hepatic Glucose and Amino Acid Content That Correlate with Fetal Organ Weights in a Mouse Model of Fetal Alcohol Spectrum Disorders"],"prefix":"10.3390","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6775-3486","authenticated-orcid":false,"given":"Nipun","family":"Saini","sequence":"first","affiliation":[{"name":"UNC Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Manjot S.","family":"Virdee","sequence":"additional","affiliation":[{"name":"UNC Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9811-1029","authenticated-orcid":false,"given":"Kaylee K.","family":"Helfrich","sequence":"additional","affiliation":[{"name":"UNC Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA"},{"name":"Department of Nutrition, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5280-9253","authenticated-orcid":false,"given":"Sze Ting Cecilia","family":"Kwan","sequence":"additional","affiliation":[{"name":"UNC Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sandra M.","family":"Mooney","sequence":"additional","affiliation":[{"name":"UNC Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA"},{"name":"Department of Nutrition, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Susan M.","family":"Smith","sequence":"additional","affiliation":[{"name":"UNC Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA"},{"name":"Department of Nutrition, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2022,3,5]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"675","DOI":"10.3945\/an.113.004846","article-title":"Nutrition implications for fetal alcohol spectrum disorder","volume":"5","author":"Young","year":"2014","journal-title":"Adv. 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