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dc.contributor.authorNeal, Elliott S
dc.contributor.authorHofstee, Pierre
dc.contributor.authorAskew, Montana R
dc.contributor.authorKent, Nykola L
dc.contributor.authorBartho, Lucy A
dc.contributor.authorPerkins, Anthony V
dc.contributor.authorCuffe, James SM
dc.date.accessioned2021-04-14T05:04:24Z
dc.date.available2021-04-14T05:04:24Z
dc.date.issued2021
dc.identifier.issn2051-817X
dc.identifier.doi10.14814/phy2.14785
dc.identifier.urihttp://hdl.handle.net/10072/403741
dc.description.abstractSelenium deficiency during pregnancy can impair fetal development and predispose offspring to thyroid dysfunction. Given that key selenoproteins are highly expressed in the kidney and that poor thyroid health can lead to kidney disease, it is likely that kidney function may be impaired in offspring of selenium-deficient mothers. This study utilized a mouse model of maternal selenium deficiency to investigate kidney protein glycation, mitochondrial adaptations, and urinary excretion in offspring. Female C57BL/6 mice were fed control (>190 µg selenium/kg) or low selenium (<50 µg selenium/kg) diets four weeks prior to mating, throughout gestation, and lactation. At postnatal day (PN) 170, offspring were placed in metabolic cages for 24 hr prior to tissue collection at PN180. Maternal selenium deficiency did not impact selenoprotein antioxidant activity, but increased advanced glycation end products in female kidneys. Male offspring had reduced renal Complex II and Complex IV protein levels and lower 24 hr urine flow. Although renal aquaporin 2 (Aqp2) and arginine vasopressin receptor 2 (Avpr2) mRNA were not altered by maternal selenium deficiency, a correlation between urine flow and plasma free T4 concentrations in male but not female offspring suggests that programed thyroid dysfunction may be mediating impaired urine flow. This study demonstrates that maternal selenium deficiency can lead to long-term deficits in kidney parameters that may be secondary to impaired thyroid dysfunction. Considering the significant burden of renal dysfunction as a comorbidity to metabolic diseases, improving maternal selenium intake in pregnancy may be one simple measure to prevent lifelong disease.
dc.description.peerreviewedYes
dc.languageeng
dc.publisherWiley
dc.relation.ispartofpagefrome14785
dc.relation.ispartofissue6
dc.relation.ispartofjournalPhysiological Reports
dc.relation.ispartofvolume9
dc.subject.fieldofresearchZoology
dc.subject.fieldofresearchClinical sciences
dc.subject.fieldofresearchMedical physiology
dc.subject.fieldofresearchcode3109
dc.subject.fieldofresearchcode3202
dc.subject.fieldofresearchcode3208
dc.subject.keywordsDOHaD
dc.subject.keywordsfetal programing
dc.subject.keywordsmaternal diet
dc.subject.keywordsoffspring kidney
dc.subject.keywordsselenium
dc.titleMaternal selenium deficiency in mice promotes sex-specific changes to urine flow and renal expression of mitochondrial proteins in adult offspring
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationNeal, ES; Hofstee, P; Askew, MR; Kent, NL; Bartho, LA; Perkins, AV; Cuffe, JSM, Maternal selenium deficiency in mice promotes sex-specific changes to urine flow and renal expression of mitochondrial proteins in adult offspring., Physiol Rep, 2021, 9 (6), pp. e14785
dcterms.dateAccepted2021-02-11
dcterms.licensehttps://creativecommons.org/licenses/by/4.0/
dc.date.updated2021-04-13T22:56:01Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
gro.hasfulltextFull Text
gro.griffith.authorPerkins, Anthony V.
gro.griffith.authorBartho, Lucy A.
gro.griffith.authorHofstee, Pierre D.
gro.griffith.authorCuffe, James S.


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