Abstract
The essential micronutrient selenium (Se) provides antioxidant defense and supports numerous biological functions. Obtained through dietary intake, Se is incorporated into selenoproteins via the amino acid, selenocysteine (Sec). Mice with genetic deletion of the Se carrier, selenoprotein P (SELENOP), and the Se recycling enzyme selenocysteine lyase (SCLY), suffer from sexually dimorphic neurological deficits and require Se supplementation for viability. These impairments are more pronounced in males and are exacerbated by dietary Se restriction. We report here that, by 10 weeks of age, female Selenop/Scly double knockout (DKO) mice supplemented with 1 mg/ml sodium selenite in drinking water develop signs of hyper-adiposity not seen in male DKO mice. Unexpectedly, this metabolic phenotype can be reversed by removing Se from the drinking water at post-natal day 22, just prior to puberty. Restricting access to Se at this age prevents excess body weight gain and restriction from either post-natal day 22 or 37 reduces gonadal fat deposits. These results provide new insight into the sex-dependent relationship between Se and metabolic homeostasis.
Highlights
Selenium (Se) has been implicated in a wide range of biological functions that are critical for human health [1]
white adipose tissue (WAT) deposits were significantly heavier in female double knockout (DKO) mice compared to WT controls (Figures 1B,C), an effect that was not observed in male DKOSe mice
Total body weight was significantly lower in female DKO when Se water was removed at post-natal day 22 (P22) compared to female DKO mice with constant Se supplementation (Figure 2A)
Summary
Selenium (Se) has been implicated in a wide range of biological functions that are critical for human health [1]. This essential trace element is translationally incorporated into selenoproteins, as the amino acid, selenocysteine (Sec). Following absorption by the gut and transport to the liver via the portal vein, Se is used to synthesize SELENOP, which contains multiple Sec residues. After being secreted into the bloodstream, SELENOP is taken up by target tissues to be catabolized intracellularly. Proper utilization of the delivered Sec residues is dependent on SCLY, which catalyzes the breakdown of Sec into selenide, to be used for de novo selenoprotein biosynthesis [3]
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