{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T22:15:22Z","timestamp":1783548922979,"version":"3.55.0"},"reference-count":111,"publisher":"Wiley","issue":"21","license":[{"start":{"date-parts":[[2023,11,23]],"date-time":"2023-11-23T00:00:00Z","timestamp":1700697600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000024","name":"Canadian Institutes of Health Research","doi-asserted-by":"publisher","award":["PJT-148 712"],"award-info":[{"award-number":["PJT-148 712"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2024,11]]},"abstract":"<jats:sec><jats:title>Abstract<\/jats:title><jats:p>Babies born with fetal growth restriction (FGR) are at higher risk of developing cardiometabolic diseases across the life course. The reduction in substrate supply to the developing fetus that causes FGR not only alters cardiac growth and structure but may have deleterious effects on metabolism and function. Using a sheep model of placental restriction to induce FGR, we investigated key cardiac metabolic and functional markers that may be altered in FGR. We also employed phase\u2010contrast magnetic resonance imaging MRI to assess left ventricular cardiac output (LVCO) as a measure of cardiac function. We hypothesized that signalling molecules involved in cardiac fatty acid utilisation and contractility would be impaired by FGR and that this would have a negative impact on LVCO in the late gestation fetus. Key glucose (GLUT4 protein) and fatty acid (<jats:italic>FATP<\/jats:italic>, <jats:italic>CD36<\/jats:italic> gene expression) substrate transporters were significantly reduced in the hearts of FGR fetuses. We also found reduced mitochondrial numbers as well as abundance of electron transport chain complexes (complexes II and IV). These data suggest that FGR diminishes metabolic and mitochondrial capacity in the fetal heart; however, alterations were not correlated with fetal LVCO. Overall, these data show that FGR alters fetal cardiac metabolism in late gestation. If sustained <jats:italic>ex utero<\/jats:italic>, this altered metabolic profile may contribute to poor cardiac outcomes in FGR\u2010born individuals after birth.\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp15835-gra-0001-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p><\/jats:sec><jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Around the time of birth, substrate utilisation in the fetal heart switches from carbohydrates to fatty acids. However, the effect of fetal growth restriction (FGR) on this switch, and thus the ability of the fetal heart to effectively metabolise fatty acids, is not fully understood.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Using a sheep model of early onset FGR, we observed significant downregulation in mRNA expression of fatty acid receptors <jats:italic>CD36<\/jats:italic> and <jats:italic>FABP<\/jats:italic> in the fetal heart. FGR fetuses also had significantly lower cardiac mitochondrial abundance than controls.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>There was a reduction in abundance of complexes II and IV within the electron transport chain of the FGR fetal heart, suggesting altered ATP production.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>This indicates reduced fatty acid metabolism and mitochondrial function in the heart of the FGR fetus, which may have detrimental long\u2010term implications and contribute to increased risk of cardiovascular disease later in life.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1113\/jp285572","type":"journal-article","created":{"date-parts":[[2023,11,25]],"date-time":"2023-11-25T00:46:29Z","timestamp":1700873189000},"page":"5901-5922","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Reduced <i>in utero<\/i> substrate supply decreases mitochondrial abundance and alters the expression of metabolic signalling molecules in the fetal sheep heart"],"prefix":"10.1113","volume":"602","author":[{"given":"Catherine G.","family":"Dimasi","sequence":"first","affiliation":[{"name":"Early Origins of Adult Health Research Group Health and Biomedical Innovation UniSA: Clinical and Health Sciences University of South Australia  Adelaide South Australia Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jack R. 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