Regulation of Intracellular Thyroid Hormone Concentrations in the Fetus

Obregón, Marı́a Jesús; Oña, Carmen Ruiz de; Rey, Francisco Escobar del; Escobar, Gabriella Morreale de

doi:10.1007/978-1-4684-7580-7_6

Cited by 5 publications

(1 citation statement)

References 38 publications

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“…Iodine is a constituent of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3), which are essential to human functioning because they influence skeletal maturation and the development of the central nervous system and regulate many other physiological processes [32][33][34]. Iodine deficiency in adults and children is usually characterized by low levels of T4 and high levels of thyroid-stimulating hormone (TSH) [35][36][37][38][39].…”

Section: Iodine Deficiencymentioning

confidence: 99%

Effects of Health and Nutrition on Cognitive and Behavioural Development in Children in the First Three Years of Life: Part 2: Infections and Micronutrient Deficiencies: Iodine, Iron, and Zinc

1999

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The following paper and its accompanying paper (Grantham-McGregor SM, et al. Effects of health and nutrition on cognitive and behavioural development in children in the first three years of life. Part 1: Low birthweight, breastfeeding, and protein-energy malnutrition. Food Nutr Bull 1999;20:53-75) review the literature on the conditions that are prevalent and considered to be likely to affect child development and are therefore of public health importance. The reviews are selective, and we have generally focused on recent work, particularly in areas that remain controversial. The reviews are restricted to nutritional and health insults that are important in the first three years of life. Where possible, we have discussed the better studies. This paper considers the effects of infections and the major micronutrient deficiencies: iodine, iron, and zinc.

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Section: Iodine Deficiencymentioning

confidence: 99%

Effects of Health and Nutrition on Cognitive and Behavioural Development in Children in the First Three Years of Life: Part 2: Infections and Micronutrient Deficiencies: Iodine, Iron, and Zinc

1999

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Thyroid hormones and their effects: a new perspective

2000

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The thyroid hormones are very hydrophobic and those that exhibit biological activity are 3',5',3,5-ltetraiodothyronine (T4), 3',5,3-l-triiodothyronine (T3), 3',5',3-l-triiodothyronine (rT3) and 3,5,-ldiiodothyronine (3,5-T2). At physiological pH, dissociation of the phenolic -OH group of these iodothyronines is an important determinant of their physical chemistry that impacts on their biological effects. When non-ionized these iodothyronines are strongly amphipathic. It is proposed that iodothyronines are normal constituents of biological membranes in vertebrates. In plasma of adult vertebrates, unbound T4 and T3 are regulated in the picomolar range whilst protein-bound T4 and T3 are maintained in the nanomolar range. The function of thyroid-hormone-binding plasma proteins is to ensure an even distribution throughout the body. Various iodothyronines are produced by three types of membrane-bound cellular deiodinase enzyme systems in vertebrates. The distribution of deiodinases varies between tissues and each has a distinct developmental profile. Thyroid hormones have many effects in vertebrates. It is proposed that there are several modes of action of these hormones. (1) The nuclear receptor mode is especially important in the thyroid hormone axis that controls plasma and cellular levels of these hormones. (2) These hormones are strongly associated with membranes in tissues and normally rigidify these membranes. (3) They also affect the acyl composition of membrane bilayers and it is suggested that this is due to the cells responding to thyroidhormone-induced membrane rigidification. Both their immediate effects on the physical state of membranes and the consequent changes in membrane composition result in several other thyroid hormone effects. Effects on metabolism may be due primarily to membrane acyl changes. There are other actions of thyroid hormones involving membrane receptors and influences on cellular interactions with the extracellular matrix. The effects of thyroid hormones are reviewed and appear to be combinations of these various modes of action. During development, vertebrates show a surge in T4 and other thyroid hormones, as well as distinctive profiles in the appearance of the deiodinase enzymes and nuclear receptors. Evidence from the use of analogues supports multiple modes of action. Re-examination of data from the early 1960s supports a membrane action. Findings from receptor 'knockout' mice supports an important role for receptors in the development of the thyroid axis. These iodothyronines may be better thought of as 'vitamone'-like molecules than traditional hormonal messengers. ABSTRACT The thyroid hormones are very hydrophobic and those that exhibit biological activity are 3h,5h,3,5--tetraiodothyronine (T4), 3h,5,3--triiodothyronine (T3), 3h,5h,3--triiodothyronine (rT3) and 3,5,--diiodothyronine (3,5-T2). At physiological pH, dissociation of the phenolic kOH group of these iodothyronines is an important determinant of their physical chemistry that impacts on their biological ...

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Effects of iodine deficiency on thyroid hormone metabolism and the brain in fetal rats: the role of the maternal transfer of thyroxin

Escobar

Obregón

Calvo

et al. 1993

The American Journal of Clinical Nutrition

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Thyroid hormones, thyroxin (T4) and 3,5,3'-triiodothyronine (T3), of maternal origin, are available to the mammalian embryo early in development. However, after the onset of fetal thyroid function, they are of both fetal and maternal origin. Maternal T4 has a protective effect on the fetal brain in cases of congenital hypothyroidism. In severe iodine deficiency, maternal T4 is low, although T3 is normal; the developing embryo is markedly T4-deficient; and T3 deficiency increases with gestational age. In contrast to mechanisms in the hypothyroid fetus from a normal mother, the low T4 of the iodine-deficient mother prevents any protective effects on the fetal brain. Thyroid hormone deficiency of the iodine-deficient fetus, including the brain, is more severe and prolonged than it is in the cases of maternal or fetal thyroid failures. These findings may help to explain the relationship between severe maternal hypothyroxinemia and the severe central nervous system damage of the neurological endemic cretin.

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Regulation of Intracellular Thyroid Hormone Concentrations in the Fetus

Cited by 5 publications

References 38 publications

Effects of Health and Nutrition on Cognitive and Behavioural Development in Children in the First Three Years of Life: Part 2: Infections and Micronutrient Deficiencies: Iodine, Iron, and Zinc

Effects of Health and Nutrition on Cognitive and Behavioural Development in Children in the First Three Years of Life: Part 2: Infections and Micronutrient Deficiencies: Iodine, Iron, and Zinc

Thyroid hormones and their effects: a new perspective

Effects of iodine deficiency on thyroid hormone metabolism and the brain in fetal rats: the role of the maternal transfer of thyroxin

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