<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Strobel KM</submitter><funding>University of California Los Angeles Children&amp;amp;apos;s Discovery and Innovation Institute, Department of Pediatrics</funding><funding>NIDDK NIH HHS</funding><funding>U.S. Department of Health &amp;amp; Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases</funding><pagination>44-51</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9840659</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>43(1)</volume><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Maternal body composition may influence fetal body composition.&lt;h4>Objective&lt;/h4>The objective of this pilot study was to investigate the relationship between maternal and fetal body composition.&lt;h4>Methods&lt;/h4>Three pregnant women cohorts were studied: healthy, gestational diabetes (GDM), and fetal growth restriction (FGR). Maternal body composition (visceral adipose tissue volume (VAT), subcutaneous adipose tissue volume (SAT), pancreatic and hepatic proton-density fat fraction (PDFF) and fetal body composition (abdominal SAT and hepatic PDFF) were measured using MRI between 30 to 36 weeks gestation.&lt;h4>Results&lt;/h4>Compared to healthy and FGR fetuses, GDM fetuses had greater hepatic PDFF (5.2 [4.2, 5.5]% vs. 3.2 [3, 3.3]% vs. 1.9 [1.4, 3.7]%, p = 0.004). Fetal hepatic PDFF was associated with maternal SAT (r = 0.47, p = 0.02), VAT (r = 0.62, p = 0.002), and pancreatic PDFF (r = 0.54, p = 0.008). When controlling for maternal SAT, GDM increased fetal hepatic PDFF by 0.9 ([0.51, 1.3], p = 0.001).&lt;h4>Conclusion&lt;/h4>In this study, maternal SAT, VAT, and GDM status were positively associated with fetal hepatic PDFF.</pubmed_abstract><journal>Journal of perinatology : official journal of the California Perinatal Association</journal><pubmed_title>Pregnancies complicated by gestational diabetes and fetal growth restriction: an analysis of maternal and fetal body composition using magnetic resonance imaging.</pubmed_title><pmcid>PMC9840659</pmcid><funding_grant_id>R01 DK124417</funding_grant_id><funding_grant_id>R01-124417-01</funding_grant_id><pubmed_authors>Strobel KM</pubmed_authors><pubmed_authors>Calkins KL</pubmed_authors><pubmed_authors>Kafali SG</pubmed_authors><pubmed_authors>Masamed R</pubmed_authors><pubmed_authors>Artura AM</pubmed_authors><pubmed_authors>Elashoff D</pubmed_authors><pubmed_authors>Shih SF</pubmed_authors><pubmed_authors>Wu HH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pregnancies complicated by gestational diabetes and fetal growth restriction: an analysis of maternal and fetal body composition using magnetic resonance imaging.</name><description>&lt;h4>Introduction&lt;/h4>Maternal body composition may influence fetal body composition.&lt;h4>Objective&lt;/h4>The objective of this pilot study was to investigate the relationship between maternal and fetal body composition.&lt;h4>Methods&lt;/h4>Three pregnant women cohorts were studied: healthy, gestational diabetes (GDM), and fetal growth restriction (FGR). Maternal body composition (visceral adipose tissue volume (VAT), subcutaneous adipose tissue volume (SAT), pancreatic and hepatic proton-density fat fraction (PDFF) and fetal body composition (abdominal SAT and hepatic PDFF) were measured using MRI between 30 to 36 weeks gestation.&lt;h4>Results&lt;/h4>Compared to healthy and FGR fetuses, GDM fetuses had greater hepatic PDFF (5.2 [4.2, 5.5]% vs. 3.2 [3, 3.3]% vs. 1.9 [1.4, 3.7]%, p = 0.004). Fetal hepatic PDFF was associated with maternal SAT (r = 0.47, p = 0.02), VAT (r = 0.62, p = 0.002), and pancreatic PDFF (r = 0.54, p = 0.008). When controlling for maternal SAT, GDM increased fetal hepatic PDFF by 0.9 ([0.51, 1.3], p = 0.001).&lt;h4>Conclusion&lt;/h4>In this study, maternal SAT, VAT, and GDM status were positively associated with fetal hepatic PDFF.</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-04T00:02:53.64Z</modification><creation>2025-04-04T00:02:53.64Z</creation></dates><accession>S-EPMC9840659</accession><cross_references><pubmed>36319757</pubmed><doi>10.1038/s41372-022-01549-5</doi></cross_references></HashMap>