Impact of restriction of placental and fetal growth on expression of 11b-hydroxysteroid dehydrogenase type 1 and type 2 messenger ribonucleic acid in the liver, kidney, and adrenal of the sheep fetus

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dc.contributor.authorMcMillen, I.
dc.contributor.authorWarnes, K.
dc.contributor.authorAdams, M.
dc.contributor.authorRobinson, J.
dc.contributor.authorOwens, J.
dc.contributor.authorCoulter, C.
dc.date.issued2000
dc.description.abstractWe have investigated the effects of fetal growth restriction, induced by restriction of placental growth and function (PR), on 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD-1) and 11betaHSD-2 messenger RNA (mRNA) expression in fetal tissues in the sheep, using Northern blot analysis. Fetal liver, kidney, and adrenals were collected from normally grown fetuses at 90 days (n = 6), 125 days (n = 6), and 141-145 days (n = 7) and from PR fetuses at 141-145 days (n = 6). Expression of 11betaHSD-1 mRNA in the fetal liver increased significantly between 125 days (7.4+/-0.8) and 141-145 days gestation (27+/-5.3). There was also an approximately 2-fold increase in the ratio of 11betaHSD-1 mRNA/18S rRNA expression in the PR group (53.8+/-7.9) compared with that in control animals at 141-145 days gestation. There was a significant decrease in 11betaHSD-2 mRNA in fetal adrenals between 125 days (41.6+/-2.4) and 141-145 days (26.7+/-1.1) gestation, but there was no effect of PR on the expression of adrenal 11betaHSD-2 mRNA. 11betaHSD-2 mRNA expression in the fetal kidney increased between 90 days (16.8+/-1.7) and 141-145 days gestation (31.7+/-4.3), but there was no effect of PR on the levels of 11betaHSD-2 mRNA in the fetal kidney. In summary, 11betaHSD-2 mRNA is differentially regulated in the fetal adrenal and kidney in the sheep fetus during late gestation. There is also a specific increase in the expression of 11betaHSD-1 mRNA in the liver of growth-restricted fetuses in late gestation. This suggests that there is increased hepatic exposure to cortisol in the growth-restricted fetus, which may be important in the reprogramming of hepatic physiology that occurs after growth restriction in utero.
dc.identifier.citationEndocrinology, 2000; 141(2):539-543
dc.identifier.doi10.1210/endo.141.2.7338
dc.identifier.issn0013-7227
dc.identifier.issn1945-7170
dc.identifier.orcidRobinson, J. [0000-0002-4515-6039]
dc.identifier.orcidOwens, J. [0000-0002-7498-1353]
dc.identifier.urihttp://hdl.handle.net/2440/11804
dc.language.isoen
dc.publisherEndocrine Soc
dc.source.urihttps://doi.org/10.1210/en.141.2.539
dc.subjectLiver
dc.subjectKidney
dc.subjectAdrenal Glands
dc.subjectPlacenta
dc.subjectAnimals
dc.subjectSheep
dc.subjectFetal Growth Retardation
dc.subjectBody Weight
dc.subjectIsoenzymes
dc.subjectHydroxysteroid Dehydrogenases
dc.subject11-beta-Hydroxysteroid Dehydrogenase Type 1
dc.subjectRNA, Messenger
dc.subjectTranscription, Genetic
dc.subjectGene Expression Regulation, Developmental
dc.subjectGene Expression Regulation, Enzymologic
dc.subjectEmbryonic and Fetal Development
dc.subjectGestational Age
dc.subjectPregnancy
dc.subjectFemale
dc.titleImpact of restriction of placental and fetal growth on expression of 11b-hydroxysteroid dehydrogenase type 1 and type 2 messenger ribonucleic acid in the liver, kidney, and adrenal of the sheep fetus
dc.typeJournal article
pubs.publication-statusPublished

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