No abstract

The German, Austrian and Swiss nutrition societies are the joint editors of the 'reference values for nutrient intake'. They have revised the reference values for the intake of selenium and published them in February 2015. The saturation of selenoprotein P (SePP) in plasma is used as a criterion for the derivation of reference values for selenium intake in adults. For persons from selenium-deficient regions (China) SePP saturation was achieved with a daily intake of 49μg of selenium. When using the reference body weights the D-A-CH reference values are based upon, the resulting estimated value for selenium intake is 70μg/day for men and 60μg/day for women. The estimated value for selenium intake for children and adolescents is extrapolated using the estimated value for adults in relation to body weight. For infants aged 0 to under 4 months the estimated value of 10μg/day was derived from the basis of selenium intake via breast milk. For infants aged 4 to under 12 months this estimated value was used and taking into account the differences regarding body weight an estimated value of 15μg/day was derived. For lactating women compared to non-lactating women a higher reference value of 75μg/day is indicated due to the release of selenium with breast milk. The additional selenium requirement for pregnant women is negligible, so that no increased reference value is indicated.

Selenium is an essential micronutrient. Its recommended daily allowance is not attained by a significant proportion of the population in many countries and its intake has been suggested to affect colorectal carcinogenesis. Therefore, microarrays were used to determine how both selenoprotein and global gene expression patterns in the mouse colon were affected by marginal selenium deficiency comparable to variations in human dietary intakes. Two groups of 12 mice each were fed a selenium-deficient (0.086 mg Se/kg) or a selenium-adequate (0.15 mg Se/kg) diet. After 6 wk, plasma selenium level, liver, and colon glutathione peroxidase (GPx) activity in the deficient group was 12, 34, and 50%, respectively, of that of the adequate group. Differential gene expression was analysed with mouse 44K whole genome microarrays. Pathway analysis by GenMAPP identified the protein biosynthesis pathway as most significantly affected, followed by inflammation, Delta-Notch and Wnt pathways. Selected gene expression changes were confirmed by quantitative real-time PCR. GPx1 and the selenoproteins W, H, and M, responded significantly to selenium intake making them candidates as biomarkers for selenium status. Thus, feeding a marginal selenium-deficient diet resulted in distinct changes in global gene expression in the mouse colon. Modulation of cancer-related pathways may contribute to the higher susceptibility to colon carcinogenesis in low selenium status.

ScopeThe SCFA acetate (Ac) and propionate (Pr) are major fermentation products of dietary fibers and provide additional energy to the host. We investigated short‐ and long‐term effects of dietary Ac and Pr supplementation on diet‐induced obesity and hepatic lipid metabolism.Methods and resultsC3H/HeOuJ mice received high‐fat (HF) diets supplemented with 5% SCFA in different Ac:Pr ratios, a high acetate (HF‐HAc; 2.5:1 Ac:Pr) or high Pr ratio (HF‐HPr; 1:2.5 Ac:Pr) for 6 or 22 weeks. Control diets (low‐fat (LF), HF) contained no SCFA. SCFA did not affect body composition but reduced hepatic gene and protein expression of lipogenic enzymes leading to a reduced hepatic triglyceride concentration after 22 weeks in HF‐HPr mice. Analysis of long‐chain fatty acid composition (liver and plasma phospholipids) showed that supplementation of both ratios led to a lower ω6:ω3 ratio. Pr directly led to increased odd‐chain fatty acid (C15:0, C17:0) formation as confirmed in vitro using HepG2 cells. Remarkably, plasma C15:0 was correlated with the attenuation of HF diet‐induced insulin resistance.ConclusionDependent on the Ac:Pr ratio, especially odd‐chain fatty acid formation and insulin sensitivity are differentially affected, indicating the importance of Pr.

Localization of GPx2, the gastrointestinal form of glutathione peroxidases (GPx), in the intestinal crypt epithelium points to a specific but so far unknown function of this particular GPx. Therefore, consequences of a GPx2 knockout were tested in mice fed a selenium-restricted, -adequate or -supplemented diet. An unexpected increase in total GPx activity was found throughout the intestine in selenium-fed GPx2 knockout animals. Immunohistochemistry revealed a strong increase of GPx1 in colon and ileum especially in crypt bases where typically GPx2 is localized. GPx1 mRNA was not enhanced in GPx2 KO, indicating that up-regulation most likely occurs at a translational level. Loss of GPx2 was accompanied by an increase of apoptotic cells at colonic crypt bases, an area essential for the self-renewal of the intestinal epithelium, particularly under selenium-restriction. Additionally mitotic cells increased in the middle parts of the crypts, indicating an extension of the proliferative area. The findings corroborate a role of GPx2 in regulating mucosal homeostasis. In GPx2 KO mice, a rise of GPx1 can only partially compensate GPx2 even under selenium-supplementation, indicating that GPx2 is the major anti-apoptotic GPx in the colon. This data explains why spontaneous ileocolitis becomes only manifested if both, gpx2 and gpx1 are deleted.