Abstract

Evidence that selenium (Se) affects the risk of type-2 diabetes (T2D) is conflicting with observational studies showing both lower and higher risk or prevalence linked to higher Se status. Importantly, however, a post-hoc analysis of the NPC trial carried out in the US showed a significantly increased risk of T2D in those supplemented with Se (200 &956;g/day as Se-yeast), the increased risk being driven by those in the highest tertile of plasma selenium at baseline (>121.6 &956;g/L). Stored plasma samples from the UK PRECISE Pilot study, in which 501 elderly volunteers were randomly assigned to a six-month treatment with 100, 200 or 300 µg Se/d as high-Se or placebo yeast, provided an opportunity to investigate the impact of Se supplementation on the risk of T2D in a lower-Se population. Plasma adiponectin concentration, a recognised independent predictor of T2D risk, was the biomarker chosen as the plasma samples were non-fasted, precluding the measurement of glucose or insulin. Adiponectin concentration was measured at baseline and at the six-month follow-up by ELISA in 473 participants who had one or both plasma samples available. Mean plasma Se increased significantly from baseline in all Se-supplemented groups. Multivariable linear regression based on log-transformed adiponectin data showed a cross-sectional inverse association between plasma Se and adiponectin concentration at baseline. However, results from linear mixed models on untransformed and log-transformed adiponectin concentrations, adjusted for study centre, showed no effect of Se supplementation on adiponectin concentration. Study limitations were the high variability in baseline adiponectin concentrations in the population, the short duration of supplementation and the narrow age range of the participants (60-74 yr). In conclusion, these findings are reassuring as they suggest absence of harm of selenium supplementation in terms of diabetes risk in a lower-Se population.

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