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Mallonee D.H.,Alltech Center for Animal Nutrigenomics and Applied Animal Nutrition | Crowdus C.A.,Alltech Center for Animal Nutrigenomics and Applied Animal Nutrition | Barger J.L.,Lifegen Technologies, Llc | Dawson K.A.,Alltech Center for Animal Nutrigenomics and Applied Animal Nutrition | Power R.F.,Alltech Center for Animal Nutrigenomics and Applied Animal Nutrition
Biological Trace Element Research

Selenium is a trace element that, although toxic in higher concentrations, is essential for human and animal health. In this study, we looked at microarray-based gene expression patterns from liver and gastrocnemius tissues in mice fed either a selenium-deficient diet or diets containing sodium selenite, selenomethionine, or a yeast-derived selenium supplement. A p value cutoff of 0.01 was used to identify a select set of selenium-responsive genes that were consistently differentially expressed across three age groups of mice with both ANOVA and t test analyses. A total of 19 gene transcripts were found to be differentially expressed across the three age groups with at least one selenium-deficient/selenium-supplemented diet comparison. Of those 19 genes, 12 had been previously identified as selenoprotein-encoding genes, and four of the genes, Gpx1, Selh, Sep15, and Sepw1, were differentially expressed in both tissues, all three mouse age groups, and all three diet comparisons. Activities associated with non-selenoproteins encoded by selenium-responsive genes included transport and stress response. The selenophosphate synthetase 2 gene Sephs2 in gastrocnemius tissue and the solute carrier gene Slc48a1 in liver tissue, both up-regulated with selenium-deficient diets compared to all three selenium-supplemented diets, are previously overlooked candidates for dietary selenium marker genes. © 2010 Springer Science+Business Media, LLC. Source

Bjorndal B.,University of Bergen | Berge K.,Aker BioMarine AS | Barger J.L.,Lifegen Technologies, Llc | Berge R.K.,University of Bergen | Burri L.,Aker BioMarine AS
Journal of Functional Foods

The effect of krill powder, a mixed source of protein and n-3 polyunsaturated fatty acids from Antarctic krill (Euphausia superba), on hepatic gene expression was analyzed in CBA/J mice. Mice were fed a low-fat control diet or a 3% (w/w) krill powder low-fat diet for 3. months. Gene expression profiling on liver samples revealed that the krill powder supplemented diet modulated a large number of pathways compared to the control diet. Metabolic pathways that were down-regulated included β-oxidation, glucose metabolism, and amino acid catabolism. In contrast, the mitochondrial electron transport chain pathway was upregulated. Krill powder affected more pathways involved in protein metabolism than krill oil. Thus, a krill powder supplemented diet had potent and specific effects on energy metabolism and oxidative phosphorylation at the gene level. This indicates that krill powder supplementation could be an approach to prevent decline in mitochondrial respiratory chain function. © 2013 Elsevier Ltd. Source

Brennan K.M.,Alltech Inc. | Brennan K.M.,University of Kentucky | Crowdus C.A.,Alltech Inc. | Cantor A.H.,University of Kentucky | And 6 more authors.
Animal Reproduction Science

Selenium (Se) is an essential component of at least 25 selenoproteins involved in a multitude of physiological functions, including reproduction. However, relatively little is known about the mechanisms by which Se exerts its physiological effects in reproductive tissue. The objective of this study was to compare the effect of long-term inorganic Se (sodium selenite, SS) and organic yeast-derived Se (Sel-Plex®, SP) supplementations on tissue Se content and gene expression patterns in the oviduct of broiler-breeder hens. Hens were randomly assigned at 6 weeks of age to one of the three treatments: basal semi-purified diet (control), basal diet+0.3ppm Se as SP or basal diet+0.3ppm Se as SS. At 49 weeks, oviduct tissue from hens randomly selected from each treatment (n=7) was analyzed for Se content and gene expression profiles using the Affymetrix Chicken genome array. Gene expression data were evaluated using GeneSpring GX 10.0 (Silicon Genetics, Redwood, CA) and Ingenuity Pathways Analysis software (Ingenuity Systems, Redwood City, CA). Oviduct Se concentration was greater with Se supplementation compared with the control (P≤0.05) but did not differ between SS- and SP-supplemented groups. Gene expression analysis revealed that the quantity of gene transcripts associated with energy production and protein translation were greater in the oviduct with SP but not SS supplementation. Targets up-regulated by SP, but not SS, included genes encoding several subunits of the mitochondrial respiratory complexes, ubiquinone production and ribosomal subunits. SS hens showed a decrease in transcripts of genes involved in respiratory complexes, ATP synthesis and protein translation and metabolism in oviduct relative to control hens. In this study, although tissue Se concentrations did not differ between hens fed SS- and SP-supplemented diets, expression patterns of genes involved in energy production and protein synthesis pathways differed between treatments. These variations may partially explain the differences in reproductive performance reported in hens fed different forms of Se. © 2011 Elsevier B.V. Source

Barger J.L.,Lifegen Technologies, Llc
Annals of the New York Academy of Sciences

Adipose tissue is an active endocrine organ that responds to changes in energy balance and influences whole-body physiology. Adipose tissue dysfunction with obesity is associated with metabolic disease, neurodegeneration, inflammation, and cancer, whereas calorie restriction (CR) decreases both adiposity and disease risk. Although resveratrol does not affect obesity, it mimics long-term CR by increasing both life span in model organisms and health span in rodents. Because resveratrol's benefits in experimental animals are reminiscent of improved adipose tissue function under CR, this review synthesizes existing data to assess if resveratrol's effects may be mediated by mimicking CR in adipose tissue. In metabolically unhealthy humans, resveratrol consumption recapitulates the health benefits of CR, whereas short-term resveratrol in otherwise healthy humans mimics CR at the transcriptional, but not physiological, level. This latter observation (neutral effect of short-term resveratrol) may be protective against future disease risk; however, long-term studies in healthy humans will be needed to support this hypothesis. © 2013 New York Academy of Sciences. Source

Hiona A.,University of Florida | Sanz A.,Tampere University of Technology | Kujoth G.C.,University of Wisconsin - Madison | Pamplona R.,University of Lleida | And 13 more authors.

Background: Aging results in a progressive loss of skeletal muscle, a condition known as sarcopenia. Mitochondrial DNA (mtDNA) mutations accumulate with aging in skeletal muscle and correlate with muscle loss, although no causal relationship has been established. Methodology/Principal Findings: We investigated the relationship between mtDNA mutations and sarcopenia at the gene expression and biochemical levels using a mouse model that expresses a proofreading-deficient version (D257A) of the mitochondrial DNA Polymerase y, resulting in increased spontaneous mtDNA mutation rates. Gene expression profiling of D257A mice followed by Parametric Analysis of Gene Set Enrichment (PAGE) indicates that the D257A mutation is associated with a profound downregulation of gene sets associated with mitochondrial function. At the biochemical level, sarcopenia in D257A mice is associated with a marked reduction (35-50%) in the content of electron transport chain (ETC) complexes I, III and IV, all of which are partly encoded by mtDNA. D257A mice display impaired mitochondrial bioenergetics associated with compromised state-3 respiration, lower ATP content and a resulting decrease in mitochondrial membrane potential (ΔΨm). Surprisingly, mitochondrial dysfunction was not accompanied by an increase in mitochondrial reactive oxygen species (ROS) production or oxidative damage. Conclusions/Significance: These findings demonstrate that mutations in mtDNA can be causal in sarcopenia by affecting the assembly of functional ETC complexes, the lack of which provokes a decrease in oxidative phosphorylation, without an increase in oxidative stress, and ultimately, skeletal muscle apoptosis and sarcopenia. © 2010 Hiona et al. Source

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