Characterisation of the maternal response to chronic phase shifts during gestation in the rat: implications for fetal metabolic programming

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dc.contributor.authorVarcoe, T.
dc.contributor.authorBoden, M.
dc.contributor.authorVoultsios, A.
dc.contributor.authorSalkeld, M.
dc.contributor.authorRattanatray, L.
dc.contributor.authorKennaway, D.
dc.contributor.editorEbihara, S.
dc.date.issued2013
dc.description.abstractDisrupting maternal circadian rhythms through exposure to chronic phase shifts of the photoperiod has lifelong consequences for the metabolic homeostasis of the fetus, such that offspring develop increased adiposity, hyperinsulinaemia and poor glucose and insulin tolerance. In an attempt to determine the mechanisms by which these poor metabolic outcomes arise, we investigated the impact of chronic phase shifts (CPS) on maternal and fetal hormonal, metabolic and circadian rhythms. We assessed weight gain and food consumption of dams exposed to either CPS or control lighting conditions throughout gestation. At day 20, dams were assessed for plasma hormone and metabolite concentrations and glucose and insulin tolerance. Additionally, the expression of a range of circadian and metabolic genes was assessed in maternal, placental and fetal tissue. Control and CPS dams consumed the same amount of food, yet CPS dams gained 70% less weight during the first week of gestation. At day 20, CPS dams had reduced retroperitoneal fat pad weight (−15%), and time-of-day dependent decreases in liver weight, whereas fetal and placental weight was not affected. Melatonin secretion was not altered, yet the timing of corticosterone, leptin, glucose, insulin, free fatty acids, triglycerides and cholesterol concentrations were profoundly disrupted. The expression of gluconeogenic and circadian clock genes in maternal and fetal liver became either arrhythmic or were in antiphase to the controls. These results demonstrate that disruptions of the photoperiod can severely disrupt normal circadian profiles of plasma hormones and metabolites, as well as gene expression in maternal and fetal tissues. Disruptions in the timing of food consumption and the downstream metabolic processes required to utilise that food, may lead to reduced efficiency of growth such that maternal weight gain is reduced during early embryonic development. It is these perturbations that may contribute to the programming of poor metabolic homeostasis in the offspring.
dc.description.statementofresponsibilityTamara J. Varcoe, Michael J. Boden, Athena Voultsios, Mark D. Salkeld, Leewen Rattanatray, David J. Kennaway
dc.identifier.citationPLoS One, 2013; 8(1):1-13
dc.identifier.doi10.1371/journal.pone.0053800
dc.identifier.issn1932-6203
dc.identifier.issn1932-6203
dc.identifier.orcidVarcoe, T. [0000-0002-9462-1830]
dc.identifier.orcidVoultsios, A. [0000-0001-7525-605X]
dc.identifier.orcidKennaway, D. [0000-0002-5864-3514]
dc.identifier.urihttp://hdl.handle.net/2440/78380
dc.language.isoen
dc.publisherPublic Library of Science
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/1009877
dc.rights© 2013 Varcoe et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
dc.source.urihttps://doi.org/10.1371/journal.pone.0053800
dc.subjectLiver
dc.subjectFetus
dc.subjectPlacenta
dc.subjectAnimals
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectHormones
dc.subjectInsulin
dc.subjectGlucose Tolerance Test
dc.subjectMothers
dc.subjectGene Expression Regulation, Developmental
dc.subjectCircadian Rhythm
dc.subjectPregnancy
dc.subjectEating
dc.subjectPhotoperiod
dc.subjectFemale
dc.subjectMale
dc.subjectCircadian Clocks
dc.titleCharacterisation of the maternal response to chronic phase shifts during gestation in the rat: implications for fetal metabolic programming
dc.typeJournal article
pubs.publication-statusPublished

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