Abstract
Selenium (Se) is a micronutrient that maintains biological functions through the action of Se containing proteins known as selenoproteins. Due to the known antioxidant effects of Se, supplements containing Se have been on the rise. While Se supplementation may be beneficial for Se deficient populations, few are at risk for Se deficiency due to the transportation of food from Se-rich regions and the rise of Se-enriched foods. Alarmingly, Se supplementation may have adverse effects in people who already receive an adequate Se supply. Specifically, an increased risk of type 2 diabetes has been reported in individuals with high baseline Se levels. However, this effect was restricted to males, suggesting the relationship between Se and glucose homeostasis may be sexually dimorphic. This review will discuss the current understanding of the interaction between Se and glucose homeostasis, including any sex differences that have been described.
Highlights
Dietary Selenium (Se) is critical for the synthesis of selenoproteins, which carry out the biological functions of Se
With the exception of the skeletal muscle, glutathione peroxidase activity and thioredoxin reductase activities were largely unchanged in insulin-sensitive tissues in response to Se supplementation, suggesting selenoprotein expression was already saturated under Se adequate conditions
These results suggest the proclivity towards metabolic disease in pigs receiving supranutritional Se doses may be a result of nonspecific incorporation of
Summary
Dietary Selenium (Se) is critical for the synthesis of selenoproteins, which carry out the biological functions of Se. Two cross-sectional studies reported lower baseline Se levels to be associated with T2D incidence among elderly French men [7], as well as in samples taken from a population in southeastern Spain [8]. Se supplementation in elderly patients [16] and pregnant women [17] from the UK, who have lower baseline Se than US subjects, did not result in increased T2D risk, as determined by serum adiponectin concentration. Another source of the inconsistencies might be attributable to differences in Se source. Interesting is that the relationship between Se metabolism and glucose homeostasis appears to be sexually dimorphic, a topic that will be discussed later in this review
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