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 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.
Highlights
A healthy diet during pregnancy is essential for maternal health and optimal fetal development, with maternal diets deficient in specific nutrients known to increase the risk of chronic disease in offspring as they age (Barker, 2007)
Given that we have shown maternal selenium deficiency to alter plasma free thyroxine (T4) concentrations in adult offspring in a sex-specific manner (Hofstee, McKeating, et al, 2020), it is possible that this altered T4 may impair offspring kidney parameters differently in males and females
Maternal selenium deficiency did not alter glutathione peroxidase (GPX) or thioredoxin reductase (TXNRD) activity (Figure 1a and 1b). As these seleno- dependent antioxidants adapted to maternal selenium deficiency, we examined if this altered the non-seleno-dependent antioxidants superoxide dismutases 1 and 2 (Sod1/2)
Summary
A healthy diet during pregnancy is essential for maternal health and optimal fetal development, with maternal diets deficient in specific nutrients known to increase the risk of chronic disease in offspring as they age (Barker, 2007). Given that 47% of healthy Australians do not meet the plasma selenium concentration required for optimal GPX activity (Lymbury et al, 2008), it is likely that many women would exhibit suboptimal levels of plasma selenium around the time of conception and during pregnancy. This is concerning given the increased requirement for selenium throughout gestation. In Australia and New Zealand, the recommended daily intake of selenium is approximately 60 μg/day for nonpregnant women, with this increasing to 65 μg/day and 75 μg/day during pregnancy and lactation, respectively (Hofstee et al, 2018)
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