<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chiaratti MR</submitter><funding>Medical Research Council</funding><funding>Wellcome Trust</funding><pagination>e0130631</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4488591</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(7)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Effective fetal growth requires adequate maternal nutrition coupled to active transport of nutrients across the placenta, which, in turn requires ATP. Epidemiological and experimental evidence has shown that impaired maternal nutrition in utero results in an adverse postnatal phenotype for the offspring. Placental mitochondrial function might link maternal food intake to fetal growth since impaired placental ATP production, in response to poor maternal nutrition, could be a pathway linking maternal food intake to reduced fetal growth.&lt;h4>Method&lt;/h4>We assessed the effects of maternal diet on placental water content, ATP levels and mitochondrial DNA (mtDNA) content in mice at embryonic (E) day 18 (E18). Females maintained on either low- (LPD) or normal- (NPD) protein diet</pubmed_abstract><journal>PloS one</journal><pubmed_title>Is Placental Mitochondrial Function a Regulator that Matches Fetal and Placental Growth to Maternal Nutrient Intake in the Mouse?</pubmed_title><pmcid>PMC4488591</pmcid><funding_grant_id>MR/J010448/1</funding_grant_id><funding_grant_id>G0500695</funding_grant_id><pubmed_authors>Morten K</pubmed_authors><pubmed_authors>Chiaratti MR</pubmed_authors><pubmed_authors>Vatish M</pubmed_authors><pubmed_authors>Malik S</pubmed_authors><pubmed_authors>Macleod L</pubmed_authors><pubmed_authors>Poulton J</pubmed_authors><pubmed_authors>Rapa E</pubmed_authors><pubmed_authors>Diot A</pubmed_authors><pubmed_authors>Boyd R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Is Placental Mitochondrial Function a Regulator that Matches Fetal and Placental Growth to Maternal Nutrient Intake in the Mouse?</name><description>&lt;h4>Background&lt;/h4>Effective fetal growth requires adequate maternal nutrition coupled to active transport of nutrients across the placenta, which, in turn requires ATP. Epidemiological and experimental evidence has shown that impaired maternal nutrition in utero results in an adverse postnatal phenotype for the offspring. Placental mitochondrial function might link maternal food intake to fetal growth since impaired placental ATP production, in response to poor maternal nutrition, could be a pathway linking maternal food intake to reduced fetal growth.&lt;h4>Method&lt;/h4>We assessed the effects of maternal diet on placental water content, ATP levels and mitochondrial DNA (mtDNA) content in mice at embryonic (E) day 18 (E18). Females maintained on either low- (LPD) or normal- (NPD) protein diet</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015</publication><modification>2025-04-04T12:52:53.258Z</modification><creation>2025-04-04T12:52:53.258Z</creation></dates><accession>S-EPMC4488591</accession><cross_references><pubmed>26132581</pubmed><doi>10.1371/journal.pone.0130631</doi></cross_references></HashMap>