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Neal ES, Hofstee P, Askew MR, et al. 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):e14785doi: 10.14814/phy2.14785.
Neal, E. S., Hofstee, P., Askew, M. R., Kent, N. L., Bartho, L. A., Perkins, A. V., & Cuffe, J. S. M. (2021). Maternal selenium deficiency in mice promotes sex-specific changes to urine flow and renal expression of mitochondrial proteins in adult offspring. Physiological reports, 9(6), e14785. https://doi.org/10.14814/phy2.14785
Neal, Elliott S, et al. "Maternal selenium deficiency in mice promotes sex-specific changes to urine flow and renal expression of mitochondrial proteins in adult offspring." Physiological reports vol. 9,6 (2021): e14785. doi: https://doi.org/10.14814/phy2.14785
Neal 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 Mar;9(6):e14785. doi: 10.14814/phy2.14785. PMID: 33769708; PMCID: PMC7995548.
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Physiol Rep. 2021 Mar;9(6):e14785. doi: 10.14814/phy2.14785.

Maternal selenium deficiency in mice promotes sex-specific changes to urine flow and renal expression of mitochondrial proteins in adult offspring.

Physiological reports

Elliott S Neal, Pierre Hofstee, Montana R Askew, Nykola L Kent, Lucy A Bartho, Anthony V Perkins, James S M Cuffe

Affiliations

  1. School of Biomedical Sciences, The University of Queensland, St Lucia, QLD, Australia.
  2. School of Medical Science, Griffith University Gold Coast Campus, Southport, QLD, Australia.

PMID: 33769708 PMCID: PMC7995548 DOI: 10.14814/phy2.14785

Abstract

Selenium 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 T

© 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.

Keywords: DOHaD; fetal programing; maternal diet; offspring kidney; selenium

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