The role of the selenoprotein S (SELS) gene -105G&gt;A promoter polymorphism in inflammatory bowel disease and regulation of SELS gene expression in intestinal inflammation

Seiderer, Julia; Dambacher, Julia; Kühnlein, B.; Pfennig, Simone; Konrad, Astrid; Haller, Dirk; Göke, B.; Ochsenkühn, Thomas; Lohse, P.; Brand, Stefan Martin

doi:10.1055/s-2007-988408

Cited by 5 publications

(5 citation statements)

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“…Earlier studies indicate that overexpressing Gpx1 impaired insulin synthesis or sensitivity (36,47), whereas knockout of Gpx1 (48,50) or Sepp1 (37) genes actually improves body insulin sensitivity. In addition, Selh and Sels might also have the biochemical potential to be involved in glucose metabolism (39,40,(51)(52)(53). Although it is unclear if the upregulations of tissue Gpx1, Sepp1, Selh, and Sels detected in the present study contributed to the induced hyperinsulinemia and/or the downregulation of tissue Akt protein, our findings indicate that pigs can be used to model the possible association of high Se intake with increased risk of diabetes in humans (54).…”

Section: Discussionmentioning

confidence: 56%

Prolonged Dietary Selenium Deficiency or Excess Does Not Globally Affect Selenoprotein Gene Expression and/or Protein Production in Various Tissues of Pigs

Liu

Zhao

Zhang

et al. 2012

The Journal of Nutrition

108

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We previously determined the effects of dietary selenium (Se) deficiency or excess on mRNA abundance of 12 selenoprotein genes in pig tissues. In this study, we determined the effect of dietary Se on mRNA levels of the remaining porcine selenoprotein genes along with protein production of 4 selenoproteins (Gpx1, Sepp1, Selh, and Sels) and body glucose homeostasis. Weanling male pigs (n = 24) were fed a Se-deficient (<0.02 mg Se/kg), basal diet supplemented with 0, 0.3, or 3.0 mg Se/kg as Se-enriched yeast (Angel Yeast) for 16 wk. Although mRNA abundance of the 13 selenoproteins in 10 tissues responded to dietary Se in 3 patterns, there was no common regulation for any given gene across all tissues or for any given tissue across all genes. Dietary Se affected (P < 0.05) 2, 3, 3, 5, 6, 7, 7, and 8 selenoprotein genes in muscle, hypothalamus, liver, kidney, heart, spleen, thyroid, and pituitary, respectively. Protein abundance of Gpx1, Sepp1, Selh, and Sels in 6 tissues was regulated (P < 0.05) by dietary Se concentrations in 3 ways. Compared with those fed 0.3 mg Se/kg, pigs fed 3.0 mg Se/kg became hyperinsulinemic (P < 0.05) and had lower (P < 0.05) tissue levels of serine/threonine protein kinase. In conclusion, dietary Se exerted no global regulation of gene transcripts or protein levels of individual selenoproteins across porcine tissues. Pigs may be a good model for studying mechanisms related to the potential prodiabetic risk of high-Se intake in humans.

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Section: Discussionmentioning

confidence: 56%

Prolonged Dietary Selenium Deficiency or Excess Does Not Globally Affect Selenoprotein Gene Expression and/or Protein Production in Various Tissues of Pigs

Liu

Zhao

Zhang

et al. 2012

The Journal of Nutrition

108

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“…Two small association studies have showed no evidence that the À105G ? A SNP in the promoter of SelS affects risk of ulcerative colitis or other autoimmune inflammatory diseases (331). However, a recent study in a Japanese population has suggested the variant affects the risk of gastric cancer (338).…”

Section: F Genetics Of Selenoproteinsmentioning

confidence: 99%

Selenium in Human Health and Disease

Fairweather‐Tait

Bao

Broadley

et al. 2011

Antioxidants & Redox Signaling

1,092

820

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This review covers current knowledge of selenium in the environment, dietary intakes, metabolism and status, functions in the body, thyroid hormone metabolism, antioxidant defense systems and oxidative metabolism, and the immune system. Selenium toxicity and links between deficiency and Keshan disease and Kashin-Beck disease are described. The relationships between selenium intake/status and various health outcomes, in particular gastrointestinal and prostate cancer, cardiovascular disease, diabetes, and male fertility, are reviewed, and recent developments in genetics of selenoproteins are outlined. The rationale behind current dietary reference intakes of selenium is explained, and examples of differences between countries and/or expert bodies are given. Throughout the review, gaps in knowledge and research requirements are identified. More research is needed to improve our understanding of selenium metabolism and requirements for optimal health. Functions of the majority of the selenoproteins await characterization, the mechanism of absorption has yet to be identified, measures of status need to be developed, and effects of genotype on metabolism require further investigation. The relationships between selenium intake/status and health, or risk of disease, are complex but require elucidation to inform clinical practice, to refine dietary recommendations, and to develop effective public health policies.

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“…The polymorphism also exhibits epistasis with a −511 polymorphism of IL-1β , greatly increasing the risk of rheumatoid arthritis in individuals with both polymorphisms, although there was no correlation of polymorphisms with rheumatoid arthritis alone [141]. However, it should be noted that other studies did not find correlations of SelS polymorphisms with stroke [142], autoimmune disorders [143] or inflammatory bowel disease [144]. Although the SelS polymorphisms are not known to be directly responsible for any particular disorder, they demonstrate how altered expression of one specific selenoprotein can increase the risk of multiple disorders.…”

Section: Immune and Inflammatory Disordersmentioning

confidence: 99%

Regulation and function of selenoproteins in human disease

Bellinger

Raman

Reeves

et al. 2009

Biochemical Journal

332

279

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Selenoproteins are proteins containing selenium in the form of the 21st amino acid, selenocysteine. Members of this protein family have many diverse functions, but their synthesis is dependent on a common set of cofactors and on dietary selenium. Although the functions of many selenoproteins are unknown, several disorders involving changes in selenoprotein structure, activity or expression have been reported. Selenium deficiency and mutations or polymorphisms in selenoprotein genes and synthesis cofactors are implicated in a variety of diseases, including muscle and cardiovascular disorders, immune dysfunction, cancer, neurological disorders and endocrine function. Members of this unusual family of proteins have roles in a variety of cell processes and diseases.

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The role of the selenoprotein S (SELS) gene -105G>A promoter polymorphism in inflammatory bowel disease and regulation of SELS gene expression in intestinal inflammation

Cited by 5 publications

References 0 publications

Prolonged Dietary Selenium Deficiency or Excess Does Not Globally Affect Selenoprotein Gene Expression and/or Protein Production in Various Tissues of Pigs

Prolonged Dietary Selenium Deficiency or Excess Does Not Globally Affect Selenoprotein Gene Expression and/or Protein Production in Various Tissues of Pigs

Selenium in Human Health and Disease

Regulation and function of selenoproteins in human disease

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