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dc.contributor.authorGatford, K.en
dc.contributor.authorSimmons, R.en
dc.contributor.authorDe Blasio, M.en
dc.contributor.authorRobinson, J.en
dc.contributor.authorOwens, J.en
dc.identifier.citationPlacenta, 2010; 31(SUPPL.):S60-S65en
dc.description.abstractBeing born small due to poor growth before birth increases the risk of developing metabolic disease, including type 2 diabetes, in later life. Inadequate insulin secretion and decreasing insulin sensitivity contribute to this increased diabetes risk. Impaired placental growth, development and function are major causes of impaired fetal growth and development and therefore of IUGR. Restricted placental growth (PR) and function in non-human animals induces similar changes in insulin secretion and sensitivity as in human IUGR, making these valuable tools to investigate the underlying mechanisms and to test interventions to prevent or ameliorate the risk of disease after IUGR. Epigenetic changes induced by an adverse fetal environment are strongly implicated as causes of later impaired insulin action. These have been well-characterised in the PR rat, where impaired insulin secretion is linked to epigenetic changes at the Pdx-1 promotor and reduced expression of this transcription factor. Present research is particularly focussed on developing intervention strategies to prevent or reverse epigenetic changes, and normalise gene expression and insulin action after PR, in order to translate this to treatments to improve outcomes in human IUGR.en
dc.description.statementofresponsibilityK.L. Gatford, R.A. Simmons, M.J. De Blasio, J.S. Robinson and J.A. Owensen
dc.publisherW B Saunders Co Ltden
dc.rightsCopyright 2010 Published by IFPA and Elsevier Ltd.en
dc.subjectIUGR; Placental restriction; Diabetes; Epigenetics; Interventionsen
dc.titlePlacental programming of postnatal diabetes and impaired insulin action after IUGRen
dc.typeJournal articleen
pubs.library.collectionObstetrics and Gynaecology publicationsen
dc.identifier.orcidGatford, K. [0000-0002-2823-3004]en
dc.identifier.orcidRobinson, J. [0000-0002-4515-6039]en
dc.identifier.orcidOwens, J. [0000-0002-7498-1353]en
Appears in Collections:Obstetrics and Gynaecology publications

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