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      Scientific Opinion on Dietary Reference Values for iodine

      EFSA Journal
      Wiley-Blackwell

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          Molecular aspects of thyroid hormone actions.

          Cellular actions of thyroid hormone may be initiated within the cell nucleus, at the plasma membrane, in cytoplasm, and at the mitochondrion. Thyroid hormone nuclear receptors (TRs) mediate the biological activities of T(3) via transcriptional regulation. Two TR genes, alpha and beta, encode four T(3)-binding receptor isoforms (alpha1, beta1, beta2, and beta3). The transcriptional activity of TRs is regulated at multiple levels. Besides being regulated by T(3), transcriptional activity is regulated by the type of thyroid hormone response elements located on the promoters of T(3) target genes, by the developmental- and tissue-dependent expression of TR isoforms, and by a host of nuclear coregulatory proteins. These nuclear coregulatory proteins modulate the transcription activity of TRs in a T(3)-dependent manner. In the absence of T(3), corepressors act to repress the basal transcriptional activity, whereas in the presence of T(3), coactivators function to activate transcription. The critical role of TRs is evident in that mutations of the TRbeta gene cause resistance to thyroid hormones to exhibit an array of symptoms due to decreasing the sensitivity of target tissues to T(3). Genetically engineered knockin mouse models also reveal that mutations of the TRs could lead to other abnormalities beyond resistance to thyroid hormones, including thyroid cancer, pituitary tumors, dwarfism, and metabolic abnormalities. Thus, the deleterious effects of mutations of TRs are more severe than previously envisioned. These genetic-engineered mouse models provide valuable tools to ascertain further the molecular actions of unliganded TRs in vivo that could underlie the pathogenesis of hypothyroidism. Actions of thyroid hormone that are not initiated by liganding of the hormone to intranuclear TR are termed nongenomic. They may begin at the plasma membrane or in cytoplasm. Plasma membrane-initiated actions begin at a receptor on integrin alphavbeta3 that activates ERK1/2 and culminate in local membrane actions on ion transport systems, such as the Na(+)/H(+) exchanger, or complex cellular events such as cell proliferation. Concentration of the integrin on cells of the vasculature and on tumor cells explains recently described proangiogenic effects of iodothyronines and proliferative actions of thyroid hormone on certain cancer cells, including gliomas. Thus, hormonal events that begin nongenomically result in effects in DNA-dependent effects. l-T(4) is an agonist at the plasma membrane without conversion to T(3). Tetraiodothyroacetic acid is a T(4) analog that inhibits the actions of T(4) and T(3) at the integrin, including angiogenesis and tumor cell proliferation. T(3) can activate phosphatidylinositol 3-kinase by a mechanism that may be cytoplasmic in origin or may begin at integrin alphavbeta3. Downstream consequences of phosphatidylinositol 3-kinase activation by T(3) include specific gene transcription and insertion of Na, K-ATPase in the plasma membrane and modulation of the activity of the ATPase. Thyroid hormone, chiefly T(3) and diiodothyronine, has important effects on mitochondrial energetics and on the cytoskeleton. Modulation by the hormone of the basal proton leak in mitochondria accounts for heat production caused by iodothyronines and a substantial component of cellular oxygen consumption. Thyroid hormone also acts on the mitochondrial genome via imported isoforms of nuclear TRs to affect several mitochondrial transcription factors. Regulation of actin polymerization by T(4) and rT(3), but not T(3), is critical to cell migration. This effect has been prominently demonstrated in neurons and glial cells and is important to brain development. The actin-related effects in neurons include fostering neurite outgrowth. A truncated TRalpha1 isoform that resides in the extranuclear compartment mediates the action of thyroid hormone on the cytoskeleton.
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            The clinical significance of subclinical thyroid dysfunction.

            Subclinical thyroid disease (SCTD) is defined as serum free T(4) and free T(3) levels within their respective reference ranges in the presence of abnormal serum TSH levels. SCTD is being diagnosed more frequently in clinical practice in young and middle-aged people as well as in the elderly. However, the clinical significance of subclinical thyroid dysfunction is much debated. Subclinical hyper- and hypothyroidism can have repercussions on the cardiovascular system and bone, as well as on other organs and systems. However, the treatment and management of SCTD and population screening are controversial despite the potential risk of progression to overt disease, and there is no consensus on the thyroid hormone and thyrotropin cutoff values at which treatment should be contemplated. Opinions differ regarding tissue effects, symptoms, signs, and cardiovascular risk. Here, we critically review the data on the prevalence and progression of SCTD, its tissue effects, and its prognostic implications. We also examine the mechanisms underlying tissue alterations in SCTD and the effects of replacement therapy on progression and tissue parameters. Lastly, we address the issue of the need to treat slight thyroid hormone deficiency or excess in relation to the patient's age.
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              Global iodine status in 2011 and trends over the past decade.

              Salt iodization has been introduced in many countries to control iodine deficiency. Our aim was to assess global and regional iodine status as of 2011 and compare it to previous WHO estimates from 2003 and 2007. Using the network of national focal points of the International Council for the Control of Iodine Deficiency Disorders as well as a literature search, we compiled new national data on urinary iodine concentration (UIC) to add to the existing data in the WHO Vitamin and Mineral Nutrition Information System Micronutrients Database. The most recent data on UIC, primarily national data in school-age children (SAC), were analyzed. The median UIC was used to classify national iodine status and the UIC distribution to estimate the number of individuals with low iodine intakes by severity categories. Survey data on UIC cover 96.1% of the world's population of SAC, and since 2007, new national data are available for 58 countries, including Canada, Pakistan, the U.K., and the U.S.. At the national level, there has been major progress: from 2003 to 2011, the number of iodine-deficient countries decreased from 54 to 32 and the number of countries with adequate iodine intake increased from 67 to 105. However, globally, 29.8% (95% CI = 29.4, 30.1) of SAC (241 million) are estimated to have insufficient iodine intakes. Sharp regional differences persist; southeast Asia has the largest number of SAC with low iodine intakes (76 million) and there has been little progress in Africa, where 39% (58 million) have inadequate iodine intakes. In summary, although iodine nutrition has been improving since 2003, global progress may be slowing. Intervention programs need to be extended to reach the nearly one-third of the global population that still has inadequate iodine intakes.
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                Author and article information

                Journal
                EFSA Journal
                EFS2
                Wiley-Blackwell
                18314732
                18314732
                May 2014
                May 2014
                : 12
                : 5
                Article
                10.2903/j.efsa.2014.3660
                87fd0909-6cde-4324-93ea-f67a8f01bd83
                © 2014

                http://doi.wiley.com/10.1002/tdm_license_1

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