Talk:Abnormal Development - Iodine Deficiency: Difference between revisions

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PMID: 21167081  
PMID: 21167081  
===Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion===
J Clin Invest. 2010 Sep 1;120(9):3377-88. doi: 10.1172/JCI42113. Epub 2010 Aug 2.
Di Cosmo C, Liao XH, Dumitrescu AM, Philp NJ, Weiss RE, Refetoff S.
Department of Medicine, University of Chicago, Chicago, Illinois, USA.
The mechanism of thyroid hormone (TH) secretion from the thyroid gland into blood is unknown. Humans and mice deficient in monocarboxylate transporter 8 (MCT8) have low serum thyroxine (T4) levels that cannot be fully explained by increased deiodination. Here, we have shown that Mct8 is localized at the basolateral membrane of thyrocytes and that the serum TH concentration is reduced in Mct8-KO mice early after being taken off a treatment that almost completely depleted the thyroid gland of TH. Thyroid glands in Mct8-KO mice contained more non-thyroglobulin-associated T4 and triiodothyronine than did those in wild-type mice, independent of deiodination. In addition, depletion of thyroidal TH content was slower during iodine deficiency. After administration of 125I, the rate of both its secretion from the thyroid gland and its appearance in the serum as trichloroacetic acid-precipitable radioactivity was greatly reduced in Mct8-KO mice. Similarly, the secretion of T4 induced by injection of thyrotropin was reduced in Mct8-KO in which endogenous TSH and T4 were suppressed by administration of triiodothyronine. To our knowledge, this study is the first to demonstrate that Mct8 is involved in the secretion of TH from the thyroid gland and contributes, in part, to the low serum T4 level observed in MCT8-deficient patients.
PMID: 20679730


===The measurement, definition, aetiology and clinical consequences of neonatal transient hypothyroxinaemia===
===The measurement, definition, aetiology and clinical consequences of neonatal transient hypothyroxinaemia===

Revision as of 14:32, 30 December 2010

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Cite this page: Hill, M.A. (2024, March 29) Embryology Abnormal Development - Iodine Deficiency. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Abnormal_Development_-_Iodine_Deficiency

2010

Consuming iodine enriched eggs to solve the iodine deficiency endemic for remote areas in Thailand

Nutr J. 2010 Dec 20;9(1):68. [Epub ahead of print]

Charoensiriwatana W, Srijantr P, Teeyapant P, Wongvilairattana J.

Abstract ABSTRACT:

BACKGROUND: Evidence showed that the occurrence of iodine deficiency endemic areas has been found in every provinces of Thailand. Thus, a new pilot programme for elimination of iodine deficiency endemic areas at the community level was designed in 2008 by integrating the concept of Sufficient Economic life style with the iodine biofortification of nutrients for community consumption.

METHODS: A model of community hen egg farm was selected at an iodine deficiency endemic area in North Eastern part of Thailand. The process for the preparation of high content iodine enriched hen food was demonstrated to the farm owner with technical transfer in order to ensure the sustainability in the long term for the community. The iodine content of the produced iodine enriched hen eggs were determined and the iodine status of volunteers who consumed the iodine enriched hen eggs were monitored by using urine iodine excretion before and after the implement of iodine enrichment in the model farm.

RESULTS: The content of iodine in eggs from the model farm were 93.57 ug per egg for the weight of 55 - 60 g egg and 97.76 ug for the weight of 60 - 65 g egg. The biological active iodo-organic compounds in eggs were tested by determination of the base-line urine iodine of the volunteer villagers before and after consuming a hard boiled iodine enriched egg per volunteer at breakfast for five days continuous period in 59 volunteers of Ban Kew village, and 65 volunteers of Ban Nong Nok Kean village. The median base-line urine iodine level of the volunteers in these two villages before consuming eggs were 7.00 and 7.04 ug/dL respectively. After consuming iodine enriched eggs, the median urine iodine were raised to the optimal level at 20.76 ug/dL for Ban Kew and 13.95 ug/dL for Ban Nong Nok Kean.

CONCLUSIONS: The strategic programme for iodine enrichment in the food chain with biological iodo-organic compound from animal origins can be an alternative method to fortify iodine in the diet for Iodine Deficiency Endemic Areas at the community level in Thailand.

PMID: 21167081


Mice deficient in MCT8 reveal a mechanism regulating thyroid hormone secretion

J Clin Invest. 2010 Sep 1;120(9):3377-88. doi: 10.1172/JCI42113. Epub 2010 Aug 2.

Di Cosmo C, Liao XH, Dumitrescu AM, Philp NJ, Weiss RE, Refetoff S.

Department of Medicine, University of Chicago, Chicago, Illinois, USA.

The mechanism of thyroid hormone (TH) secretion from the thyroid gland into blood is unknown. Humans and mice deficient in monocarboxylate transporter 8 (MCT8) have low serum thyroxine (T4) levels that cannot be fully explained by increased deiodination. Here, we have shown that Mct8 is localized at the basolateral membrane of thyrocytes and that the serum TH concentration is reduced in Mct8-KO mice early after being taken off a treatment that almost completely depleted the thyroid gland of TH. Thyroid glands in Mct8-KO mice contained more non-thyroglobulin-associated T4 and triiodothyronine than did those in wild-type mice, independent of deiodination. In addition, depletion of thyroidal TH content was slower during iodine deficiency. After administration of 125I, the rate of both its secretion from the thyroid gland and its appearance in the serum as trichloroacetic acid-precipitable radioactivity was greatly reduced in Mct8-KO mice. Similarly, the secretion of T4 induced by injection of thyrotropin was reduced in Mct8-KO in which endogenous TSH and T4 were suppressed by administration of triiodothyronine. To our knowledge, this study is the first to demonstrate that Mct8 is involved in the secretion of TH from the thyroid gland and contributes, in part, to the low serum T4 level observed in MCT8-deficient patients.

PMID: 20679730

The measurement, definition, aetiology and clinical consequences of neonatal transient hypothyroxinaemia

Ann Clin Biochem. 2010 Oct 7.

Williams F, Hume R.

Clinical and Population Sciences and Education, Human Brain Development Group, Mackenzie Building, Ninewells Hospital and Medical School Campus, Kirsty Semple Way, Dundee DD2 4BF, UK. Abstract This review focuses on neonatal transient hypothyroxinaemia, a condition characterized by temporary postnatal reductions in concentrations of Total T4 or Free T4, with normal or low concentrations of thyroid stimulating hormone (TSH). There is neither an agreed quantitative definition, nor an agreed mode of measurement for the condition. Transient hypothyroxinaemia is not routinely monitored yet it is thought to affect about 50% of preterm infants; it was thought to be without long-term sequelae but observational studies indicate that neurodevelopment may be compromised. The aetiology of transient hypothyroxinaemia is complex. There are significant contributions from the withdrawal of maternal-placental thyroxine transfer, hypothalamic-pituitary-thyroid immaturity, developmental constraints on the synthesis and peripheral metabolism of iodothyronines and iodine deficiency. It is not possible to distinguish clinically, or from laboratory measurements, whether transient hypothyroxinaemia is an independent condition or simply a consequence of non-thyroidal illness and/or drug usage. An answer to this question is important because studies of thyroid hormone replacement have been instigated, with mixed results. Until the aetiology of transient hypothyroxinaemia is better understood it would seem prudent not to routinely supplement preterm infants with thyroid hormones. Iodine deficiency, non-thyroidal illness and drug usage are the most modifiable risk factors for transient hypothyroxinaemia and are the clear choices for attempts at reducing its incidence. We suggest that transient hypothyroxinaemia in preterm infants is defined as a normal or low TSH concentration in conjunction with a concentration of Total T4, that is ≤10th percentile of cord Total T4 of the equivalent gestational age had the infant remained in utero.

PMID: 20930033

A sprinkle of salt needed for Nepal's hidden hunger

Siva N. Lancet. 2010 Aug 28;376(9742):673-4. No abstract available. PMID: 20879078

Iodine deficiency in Australia: is iodine supplementation for pregnant and lactating women warranted? Comment

Anderson WP, Zhou SJ, Skeaff SA, Ryan P, Makrides M, Gallego G, Goodall S, Eastman CJ. Med J Aust. 2010 Sep 6;193(5):309; author reply 310-1. No abstract available.

In January 2010, the National Health and Medical Research Council (NHMRC) released a public statement, Iodine supplementation for pregnant and breastfeeding women.2

PMID: 20819054


Estimating the impact of mandatory fortification of bread with iodine on pregnant and post-partum women

J Epidemiol Community Health. 2010 Aug 13. [Epub ahead of print]

Mackerras D, Powers J, Boorman J, Loxton D, Giles GG.

Canberra, Australia. Abstract Background Iodine deficiency has re-emerged in Australia. Pregnant and breastfeeding women need higher iodine intakes (estimated average requirements: 160 mug/day and 190 mug/day) than non-pregnant women (100 mug/day) because iodine is critical for early infant development. The impact of iodine fortification of bread on women's iodine intake is evaluated by reproductive status using 2003 Australian Longitudinal Study on Women's Health (ALSWH) food frequency data and projected onto 1995 National Nutrition Survey (NNS) daily food consumption data for women of child-bearing age. Methods Recent iodine analyses of Australian foods were combined with reported intakes of key foods to estimate iodine intake before and after fortification for 665 pregnant, 432 zero to 6 months postpartum, 467 seven to 12 months postpartum and 7324 non-pregnant women. Differences in mean iodine intake between these groups were projected onto NNS estimates of total iodine intake for women of child-bearing age. Results Pregnant and postpartum women reported eating more bread than did non-pregnant women. Mean iodine intakes (mug/day before; and after fortification) from key foods were higher in pregnant (78; 124), 0-6 months postpartum (75; 123) and 7-12 months postpartum (71; 117) than in non-pregnant women (65; 103). Projecting ALSWH results onto the NNS yields total mean iodine intakes of 167, 167, 160 and 146 for the same groups. Conclusion Current iodine intakes are well below dietary recommendations. The impact of iodine fortification of bread would be greater for pregnant and postpartum women than has been previously estimated using general population intakes, but additional strategies to increase intakes by these groups are still needed.

PMID: 20709857


Iodine excess

Best Pract Res Clin Endocrinol Metab. 2010 Feb;24(1):107-15.

Bürgi H.

International Council for the Control of Iodine Deficiency Disorders (ICCIDD), CH-4500 Solothurn, Switzerland. hans.buergi@gmail.com Abstract Several mechanisms are involved in the maintenance of normal thyroid hormone secretion, even when iodine intake exceeds physiologic needs by a factor of 100. The sodium-iodide symporter system contributes most to this stability. Faced with an iodine excess, it throttles the transport of iodide into the thyroid cells, the rate-limiting step of hormone synthesis. Even before the iodine symporter reacts, a sudden iodine overload paradoxically blocks the second step of hormone synthesis, the organification of iodide. This so-called Wolff-Chaikoff effect requires a high (>or=10(-3) molar) intracellular concentration of iodide. The block does not last long, because after a while the sodium-iodide symporter shuts down; this allows intracellular iodide to drop below 10(-3) molar and the near-normal secretion to resume. In some susceptible individuals (e.g., after radio-iodine treatment of Graves' disease or in autoimmune thyroiditis), the sodium-iodide symporter fails to shut down, the intracellular concentration of iodide remains high and chronic hypothyroidism ensues. To complicate matters, iodine excess may also cause hyperthyroidism. The current explanation is that this happens in persons with goitres, for example, after long-standing iodine deficiency. These goitres may contain nodules carrying a somatic mutation that confers a 'constitutive' activation of the TSH receptor. Being no more under pituitary control, these nodules overproduce thyroid hormone and cause iodine-induced hyperthyroidism, when they are presented with sufficient iodine. These autonomous nodules gradually disappear from the population after iodine deficiency has been properly corrected. More recent studies suggest that chronic high iodine intake furthers classical thyroid autoimmunity (hypothyroidism and thyroiditis) and that iodine-induced hyperthyroidism may also have an autoimmune pathogenesis.

Copyright 2009 Elsevier Ltd. All rights reserved. PMID: 20172475


The impact of common micronutrient deficiencies on iodine and thyroid metabolism: the evidence from human studies

Best Pract Res Clin Endocrinol Metab. 2010 Feb;24(1):117-32.

Hess SY.

Program in International and Community Nutrition, Department of Nutrition, University of California, Davis, CA, USA. syhess@ucdavis.edu Abstract Deficiencies of micronutrients are highly prevalent in low-income countries. Inadequate intake of iodine impairs thyroid function and results in a spectrum of disorders. Other common deficiencies of micronutrients such as iron, selenium, vitamin A, and possibly zinc may interact with iodine nutrition and thyroid function. Randomised controlled intervention trials in iodine- and iron-deficient populations have shown that providing iron along with iodine results in greater improvements in thyroid function and volume than providing iodine alone. Vitamin A supplementation given alone or in combination with iodised salt can have a beneficial impact on thyroid function and thyroid size. Despite numerous studies of the effect of selenium on iodine and thyroid metabolism in animals, most published randomised controlled intervention trials in human populations failed to confirm an impact of selenium supplementation on thyroid metabolism. Little evidence is available on interactions between iodine and zinc metabolism.

Copyright 2009 Elsevier Ltd. All rights reserved. PMID: 20172476