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dc.contributor.authorDavies
dc.contributor.authorSmith
dc.contributor.authorEl-Bacha
dc.contributor.authorWooding
dc.contributor.authorForhead
dc.contributor.authorMurray
dc.contributor.authorFowden
dc.contributor.authorCamm
dc.date.accessioned2022-06-07T08:12:11Z
dc.date.available2022-06-07T08:12:11Z
dc.date.issued2022-05-31
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/337769
dc.description.abstractIn adults, glucocorticoids are stress hormones that act, partly, through actions on mitochondrial oxidative phosphorylation (OXPHOS) to increase energy availability. Before birth, glucocorticoids are primarily maturational signals that prepare the fetus for new postnatal challenges. However, the role of the normal prepartum glucocorticoid rise in preparing mitochondria for the increased postnatal energy demands remains largely unknown. This study examined the effect of physiological increases in the fetal cortisol concentration on cerebral mitochondrial OXPHOS capacity near term (~130 days gestation, term ~145 days gestation). Fetal sheep were infused with saline or cortisol for 5 days at ~0.8 of gestation before the mitochondrial content, respiratory rates, abundance of the electron transfer system proteins and OXPHOS efficiency were measured in their cortex and cerebellum. Cerebral morphology was assessed by immunohistochemistry and stereology. Cortisol treatment increased the mitochondrial content, while decreasing Complex I-linked respiration in the cerebellum. There was no effect on the cortical mitochondrial OXPHOS capacity. Cortisol infusion had regional effects on cerebral morphology, with increased myelination in the cerebrum. The findings demonstrate the importance of cortisol in regulating the cerebral mitochondrial OXPHOS capacity prenatally and have implications for infants born preterm or after glucocorticoid overexposure due to pregnancy complications or clinical treatment.
dc.languageen
dc.publisherMDPI
dc.subjectcortisol
dc.subjectfetus
dc.subjectmitochondria
dc.subjectbrain
dc.titleCortisol Regulates Cerebral Mitochondrial Oxidative Phosphorylation and Morphology of the Brain in a Region-Specific Manner in the Ovine Fetus
dc.typeArticle
dc.date.updated2022-06-07T08:12:11Z
prism.issueIdentifier6
prism.publicationNameBiomolecules
prism.volume12
dc.identifier.doi10.17863/CAM.85178
dcterms.dateAccepted2022-05-28
rioxxterms.versionofrecord10.3390/biom12060768
rioxxterms.versionVoR
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0/
dc.contributor.orcidSmith [0000-0002-6708-5470]
dc.contributor.orcidEl-Bacha [0000-0003-0809-0218]
dc.contributor.orcidCamm [0000-0003-0767-2697]
dc.identifier.eissn2218-273X
pubs.funder-project-idBiotechnology and Biological Sciences Research Council (BB/P019048/1)
pubs.funder-project-idWellcome Trust (102357)


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