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Selenium, selenoproteins and the thyroid gland: interactions in health and disease.
Nat Rev Endocrinol 2011; 8(3):160-71NR

Abstract

The trace element selenium is an essential micronutrient that is required for the biosynthesis of selenocysteine-containing selenoproteins. Most of the known selenoproteins are expressed in the thyroid gland, including some with still unknown functions. Among the well-characterized selenoproteins are the iodothyronine deiodinases, glutathione peroxidases and thioredoxin reductases, enzymes involved in thyroid hormone metabolism, regulation of redox state and protection from oxidative damage. Selenium content in selenium-sensitive tissues such as the liver, kidney or muscle and expression of nonessential selenoproteins, such as the glutathione peroxidases GPx1 and GPx3, is controlled by nutritional supply. The thyroid gland is, however, largely independent from dietary selenium intake and thyroid selenoproteins are preferentially expressed. As a consequence, no explicit effects on thyroid hormone profiles are observed in healthy individuals undergoing selenium supplementation. However, low selenium status correlates with risk of goiter and multiple nodules in European women. Some clinical studies have demonstrated that selenium-deficient patients with autoimmune thyroid disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined. The baseline selenium status of an individual could constitute the most important parameter modifying the outcome of selenium supplementation, which might primarily disrupt self-amplifying cycles of the endocrine-immune system interface rectifying the interaction of lymphocytes with thyroid autoantigens. Selenium deficiency is likely to constitute a risk factor for a feedforward derangement of the immune system-thyroid interaction, while selenium supplementation appears to dampen the self-amplifying nature of this derailed interaction.

Authors+Show Affiliations

Institute for Experimental Endocrinology, Charité-University Medicine Berlin, Südring 10, CVK, 13353 Berlin, Germany. lutz.schomburg@charite.de

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

22009156

Citation

Schomburg, Lutz. "Selenium, Selenoproteins and the Thyroid Gland: Interactions in Health and Disease." Nature Reviews. Endocrinology, vol. 8, no. 3, 2011, pp. 160-71.
Schomburg L. Selenium, selenoproteins and the thyroid gland: interactions in health and disease. Nat Rev Endocrinol. 2011;8(3):160-71.
Schomburg, L. (2011). Selenium, selenoproteins and the thyroid gland: interactions in health and disease. Nature Reviews. Endocrinology, 8(3), pp. 160-71. doi:10.1038/nrendo.2011.174.
Schomburg L. Selenium, Selenoproteins and the Thyroid Gland: Interactions in Health and Disease. Nat Rev Endocrinol. 2011 Oct 18;8(3):160-71. PubMed PMID: 22009156.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Selenium, selenoproteins and the thyroid gland: interactions in health and disease. A1 - Schomburg,Lutz, Y1 - 2011/10/18/ PY - 2011/10/20/entrez PY - 2011/10/20/pubmed PY - 2012/8/21/medline SP - 160 EP - 71 JF - Nature reviews. Endocrinology JO - Nat Rev Endocrinol VL - 8 IS - 3 N2 - The trace element selenium is an essential micronutrient that is required for the biosynthesis of selenocysteine-containing selenoproteins. Most of the known selenoproteins are expressed in the thyroid gland, including some with still unknown functions. Among the well-characterized selenoproteins are the iodothyronine deiodinases, glutathione peroxidases and thioredoxin reductases, enzymes involved in thyroid hormone metabolism, regulation of redox state and protection from oxidative damage. Selenium content in selenium-sensitive tissues such as the liver, kidney or muscle and expression of nonessential selenoproteins, such as the glutathione peroxidases GPx1 and GPx3, is controlled by nutritional supply. The thyroid gland is, however, largely independent from dietary selenium intake and thyroid selenoproteins are preferentially expressed. As a consequence, no explicit effects on thyroid hormone profiles are observed in healthy individuals undergoing selenium supplementation. However, low selenium status correlates with risk of goiter and multiple nodules in European women. Some clinical studies have demonstrated that selenium-deficient patients with autoimmune thyroid disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined. The baseline selenium status of an individual could constitute the most important parameter modifying the outcome of selenium supplementation, which might primarily disrupt self-amplifying cycles of the endocrine-immune system interface rectifying the interaction of lymphocytes with thyroid autoantigens. Selenium deficiency is likely to constitute a risk factor for a feedforward derangement of the immune system-thyroid interaction, while selenium supplementation appears to dampen the self-amplifying nature of this derailed interaction. SN - 1759-5037 UR - https://www.unboundmedicine.com/medline/citation/22009156/full_citation L2 - http://dx.doi.org/10.1038/nrendo.2011.174 DB - PRIME DP - Unbound Medicine ER -