Abstract
Selenium deficiency during the perinatal period programs metabolic dysfunction in offspring. Postnatal exercise may prevent the development of programmed metabolic disease. This study investigated the impact of selenium deficiency on offspring exercise behavior and whether this improved metabolic health. Female C57BL/6 mice were randomly allocated to control (NormalSe, >190 μg/Se/kg, n = 8) or low-selenium (LowSe, <50 μg/Se/kg, n = 8) diets from four weeks before mating. Male offspring were weaned at postnatal day (PN) twenty-four and placed on a normal chow diet. At PN60, mice were placed in cages with bi-directional running wheels and monitored until PN180. LowSe offspring had a reduced average weekly running speed and distance (p < 0.05). LowSe offspring exhibited glucose intolerance, with increased peak blood glucose (p < 0.05) and area under the curve following an intra-peritoneal injection of glucose (p < 0.05). Furthermore, mRNA expression of several selenoproteins within cardiac and skeletal muscle were increased in LowSe offspring (p < 0.05). The results indicated that selenium deficiency during development reduces exercise behavior. Furthermore, exercise does not prevent programmed glucose intolerance in low-selenium offspring. This highlights that exercise may not be the optimal intervention for metabolic disease in offspring impacted by selenium deficiency in early life.
Highlights
We have previously demonstrated that selenium deficiency in pregnancy causes growth restriction of the fetus, programs metabolic disease in offspring and causes long-term changes to selenoprotein expression [14,15]
Selenium deficiency during adult life has previously been associated with reduced muscle function [8] the impact of early-life selenium deficiency on later-life exercise capacity was unknown before this study
We have previously shown that mRNA expression of key antioxidant selenoproteins (Gpx1, Gpx3, Trxr1 and Trxr2) was decreased in maternal tissues during the period of selenium deficiency [15], but that six-month-old offspring of seleniumdeficient dams had similar expression levels compared to offspring from normal selenium mothers
Summary
Exercise and physical activity are known to stimulate beneficial physiological responses at both the cellular level and across multiple organ systems [1]. Individuals at risk of chronic disease, such as type 2 diabetes mellitus, can benefit significantly from increasing their physical activity, if they are physically capable of doing so. Regular endurance exercise causes adaptations that lead to a shift in oxidative metabolism, upregulating mitochondrial systems, enhancing oxidative capacity and substantially improving mitochondrial respiration [2]. Exercise facilitates insulin-independent glucose uptake in skeletal muscle so that it can be utilized in cellular respiratory processes [3]—this is known to occur even in individuals who are insulin-resistant and helps to restore insulin sensitivity. Increased energy utilization by tissues, such as cardiac and skeletal muscle during physical activity, is strongly impacted by several essential micronutrients [4] that help maintain optimal mitochondrial respiration and prevent excessive oxidative stress [5]. One micronutrient important to endogenous antioxidant systems is selenium [6]
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