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Maternal selenium deficiency in mice promotes sex- specific changes to urine flow and renal expression of mitochondrial proteins in adult offspring1.35 MB
Published VersionCC BY V4.0, Open Access
Journal article
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), pp.1-23
2021
PMID: 33769708
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
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.
Details
- Title
- Maternal selenium deficiency in mice promotes sex-specific changes to urine flow and renal expression of mitochondrial proteins in adult offspring
- Authors
- Elliott S Neal (Author) - The University of QueenslandPierre Hofstee (Author) - Griffith UniversityMontana R Askew (Author) - The University of QueenslandNykola L Kent (Author) - The University of QueenslandLucy A Bartho (Author) - Griffith UniversityAnthony V Perkins (Author) - Griffith UniversityJames S M Cuffe (Corresponding Author) - Griffith University
- Publication details
- Physiological Reports, Vol.9(6), pp.1-23
- Publisher
- MDPI AG
- Date published
- 2021
- DOI
- 10.14814/phy2.14785
- ISSN
- 2051-817X
- PMID
- 33769708
- Copyright note
- © 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.
- Grant note
- Griffith University Postgraduate Research Scholarship (GUPRS-NS) Australian Government's Collaborative Research Networks (CRN) program; Australian Government Allen Foundation (USA) Griffith Health Top Up Scholarship Allen Foundation, Inc. Griffith University International Postgraduate Research Scholarship (GUIPRSNS)
- Organisation Unit
- School of Health; University of the Sunshine Coast, Queensland; School of Health and Behavioural Sciences - Legacy
- Language
- English
- Record Identifier
- 99685298102621
- Output Type
- Journal article
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