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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #313845

Research Project: Health Roles of Dietary Selenium in Obesity

Location: Dietary Prevention of Obesity-related Disease Research

Title: Conditional effect of selenium on the mammalian hind gut microbiota

Author
item Taussig, David
item Combs, Gerald

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 1/15/2014
Publication Date: 3/28/2015
Citation: Taussig, D.P., Combs, G.F. 2015. Conditional effect of selenium on the mammalian hind gut microbiota [abstract]. Journal of Federation of American Societies for Experimental Biology. 29:759.2.

Interpretive Summary: Selenium (Se) status is linked to cancer risk in humans and other mammals. Because Se is used by certain microbial species which contain selenoproteins, and because hind gut microfloral composition is linked to cancer development, we proposed that supranutritional Se could reduce tumorigenisis by affecting the gut microflora. To test this hypothesis, we carried out studies of the effects of dietary Se level on the hind gut microbiota taxonomy and metabolism in two species, rats and mice. Briefly, we used metagenomic, metabolomic, and qPCR-based approaches to characterize the taxonomy and metabolic output of gut microbiota in animals fed either adequate (0.15 ppm) or high (2 ppm, known to be anticarcinogenic in these models) levels of Se. Additional independent variables included high fat, fermentable fiber (wheat bran), or insoluble fiber (cellulose), all known to affect the gut microbiome. While twenty-four microbes known to encode selenoenzymes were detected in mice, none were significantly altered by supranutritional Se feeding. Moreover, the numbers of significantly different species and metabolite abundances were below those expected through random chance within such large data sets, suggesting that the adequate level of Se is not limiting for microbial distribution or function in the mouse. However, high-Se feeding increased the proportion of Bifidobacteria in the rat, suggesting an effect on that microbial community. Questions remain regarding the effect of Se on Bifidobacteria, which are not known to have selenoproteins. These include whether this is a direct effect or one involving other species, and whether it may contribute to Se-anticarcinogenesis.

Technical Abstract: Selenium (Se) status is linked to cancer risk in humans and other mammals. Because Se is used by certain microbial species which contain selenoproteins, and because hind gut microfloral composition is linked to cancer development, we proposed that supranutritional Se could reduce tumorigenisis by affecting the gut microflora. To test this hypothesis, we carried out studies of the effects of dietary Se level on the hind gut microbiota taxonomy and metabolism in two species, rats and mice. Briefly, we used metagenomic, metabolomic, and qPCR-based approaches to characterize the taxonomy and metabolic output of gut microbiota in animals fed either adequate (0.15 ppm) or high (2 ppm, known to be anticarcinogenic in these models) levels of Se. Additional independent variables included high fat, fermentable fiber (wheat bran), or insoluble fiber (cellulose), all known to affect the gut microbiome. While twenty-four microbes known to encode selenoenzymes were detected in mice, none were significantly altered by supranutritional Se feeding. Moreover, the numbers of significantly different species and metabolite abundances were below those expected through random chance within such large data sets, suggesting that the adequate level of Se is not limiting for microbial distribution or function in the mouse. However, high-Se feeding increased the proportion of Bifidobacteria in the rat, suggesting an effect on that microbial community. Questions remain regarding the effect of Se on Bifidobacteria, which are not known to have selenoproteins. These include whether this is a direct effect or one involving other species, and whether it may contribute to Se-anticarcinogenesis.