3,5,3 - Triiodothyronine brain

Thyroid hormone receptors (THRs) are subdivided intoa and P types, each having two isoforms. In rat brain, THR, mRNA is present in hippocampus, hypothalmus, cortex, cerebellum, and amygdala. Thyroxine (l-T (284) and triiodothyronine (l-T ) (285) are endogenous ligands for the THRs. TRIAC (286) is a THR antagonist. Selective ligands for PPARs have yet to be identified (Table 16). 

Triiodothyronine (Cytomel, T3). T3 is also an effective augmenting agent. It is important to use the T3 thyroid hormone instead of thyroxine (T4). T4 is the form most often used to treat hypothyroidism, but T3 crosses from the bloodstream to the brain more easily and thus is better for treating depression. T3 is usually tolerated well and is taken at 25-50 pg/day in split doses. When taking T3, laboratory tests to check thyroid function should be performed periodically. 

The amino acids that are made available as a result of protein degradation in starvation are nsed as precursors of glucose, which is required for the brain. The decline in starvation-induced protein degradation is a result of the decreased requirement for glucose by the brain due to the increase in utilisation of ketone bodies. The qnestion arises, therefore, as to the mechanism by which the protein breakdown in muscle is reduced. Two answers, which are interdependent, have been put forward (i) decreased metabolic activity in tissues, and (ii) a decrease in the plasma level of thyroxine and hence triiodothyronine. 

Whitworth P, Kendall DA Effects of lithium on inositol phospholipid hydrolysis and inhibition of dopamine D, receptor-mediated cyclic AMP formation by carbachol in rat brain slices. J Neurochem 53 536-541, 1989 Whybrow PC The therapeutic use of triiodothyronine and high dose thyroxine in psychiatric disorder. Acta Med Austriaca 21 44-47, 1994 Whybrow PC Update on thyroid axis approaches to treatment of rapid cycling bipolar disorder. Paper presented at the annual meeting of the New Clinical Drug Evaluations Unit (NCDEU), Boca Raton, EL, May 30, 1996... 

The culture system used in this study has proven suitable for studying the regulation, especially by hormones, of myelina-tion in vitro. Initial studies (35-36), however, showed no effect of 3, 5, 3 -triiodothyronine (T,) on sulfolipid synthesis by dissociated brain cells grown on medium containing 20% calf... 

Thyrotropin-releasing hormone, or protirelin, is a tripeptide hormone found in the paraventricular nuclei of the hypothalamus as well as in other parts of the brain. TRH is secreted into the portal venous system and stimulates the pituitary to produce thyroid-stimulating hormone (TSH, thyrotropin), which in turn stimulates the thyroid to produce thyroxine (T4) and triiodothyronine (T3). TRH stimulation of thyrotropin is blocked by thyroxine and potentiated by lack of thyroxine. 

Abbreviations 3,5,3, 5 -tetraiodothyronine or thyroxine, T4 3,5,3-triiodothyronine, T, 3,3, 5 -triio-dothyronine, reverse T, or r-T3 3,5,3, 5 -tetraiodothyroacetic acid, TETRAC 3,5,3 -triiodothyroacetic acid, TRIAC 3,5-diiodotyrosine, DIT 3-monoiodotyrosine, MIT thyrotropic hormone, TSH thyreo-liberin, TRH growth hormone, GH microtubule associated proteins, MAPs TAU protein, one of the brain MAPs. 

OH-PCBs can also influence thyroxine metabolism. Some of the OH-PCBs that are retained in blood were shown to strongly inhibit sulfation of thyroxine in vitro [204-206]. As sulfation is a major regulation pathway of thyroxine in the fetus, the OH-PCBs may negatively influence the development of the fetus, and in particular fetal brain development [44]. Diodinase mediation is another pathway for thyroxine metabolism e.g., to the active hormone triiodothyronine. Hydroxylated metabolites of CB-77 were shown to inhibit triiodothyronine formation in an in vitro assay using rat hepatic microsomes [207],... 

Bilberry extract 200 mg/(kg day) administered intraperitoneally to euthyroid rats increased radiolabeled triiodothyronine (T3) transport into the brain, compared to vehicle only (21). Postulated mechanisms include central or peripheral inhibition of L-thyroxine s (T4) deiodination to T3 inhibition of T3 protein binding or enhanced T3 binding to carrier proteins in the brain capillary wall (21). Whether bilberry could interact with thyroid replacement therapy remains to be seen. 

S aij a A, Princi P, D Amico N, De Pasquale R, Costa G. Effect of Vaccinium myrtillus anthocyanins on triiodothyronine transport into brain in the rat. Pharmacol Rev 1990 22 59-60. 

Selenium is a component of all three members of the deiodinase enzyme family, the enzymes responsible for deiodination of the thyroid hormones (Kohrle 1994 St. Germain and Galton 1997). The deiodinases contain a selenocysteine at the active site, which is required for catalytic activity. There are three types of deiodinases and they differ in terms of tissue distribution, reaction kinetics, efficiency of substrate utilization, and sensitivity to inhibitors. The first to be recognized as a selenoprotein was type I iodothyronine 5 -deiodinase which converts the prohormone thyroxine (T4) to the active form, triiodothyronine (T3) and to date, studies of the effects of excess selenium have focused on this protein. Under normal circumstances the human thyroid produces only 20-30% of its hormone as T3 the remainder is T4 (a minute amount of reverse T3 (rT3) is also produced), which is largely converted to active T3 by type I deiodinase located within the liver, euthyroid pituitary, kidney, thyroid, and brain. Type I deiodinase is a membrane bound protein and, thus, its activity has not been directly measured in studies of humans supplemented with selenium. Human studies have instead measured serum levels of T3, rT3, T4, and TSH. 

Valcana, T., The role of triiodothyronine in brain development, in Neural Growth and Differentiation, Meisami, E. and Brazier, M. A. B., Eds., Raven Press, New York, 1979, 39-58. 

Margarity, M., Valcana, T., and Timiras, P. S., Thyroxine deiodination, cytoplasmic distribution and nuclear binding of thyroxine and triiodothyronine in liver and brain of young and aged rats, Mech. Ageing Dev., 29, 181, 1985. 

The thyroid gland synthesizes and releases T3 (3, 3 -triiodothyronine) and (thyroxine) which regulate protein synthesis, regulate membrane-bound enzymes and stimulate mitochondrial oxidation. T3 and also regulate fetal and infant brain development and childhood growth. T3 is more potent than T. ... 

Iodine is an essential element in humans and other mammals, which is used for the synthesis of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). These hormones play a prominent role in the metabolism of most cells of the organism and in the process of early growth and development of most organs, especially brain (Anderson et al., 2000). Besides T3 and T4, reverse T3 (rT3), monoiodotyrosine (MIT), and diiodotyrosine (DIT) are also synthesized and distributed in the body of humans and animals, but only T3 and T4 have a biological function. Iodine in the human body mainly comes through dietary and water intake, and inhalation of atmospheric iodine. Due to low concentrations of iodine in the air (10—20ng/m ), food and water intake form the major source of iodine for adults, while for infants it is milk. The concentration of iodine in foodstuffs is directly related to that in the environment where the foods come from. Iodine deficiency disorders are mainly found in places where the concentration of iodine in the soil and drinking water is very low. In the water, foodsmffs, and... 

TH plays an important role in fetal and early postnatal brain development. The pro-hormone T4 (3,3 ,5,5 -triiodothyronine) is converted in the brain to its active form, T3, or its inactive metabofite, reverse T3, mainly by the action of DI02. 

Iodine is essential for the synthesis of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4). An iodine-deficient diet results directly in decreased production of thyroid hormones, which adversely affects not only brain development, but also its functions such as attention, learning and memory. In areas with iodine deficiency, besides the occurrence of more frequent thyroid nodules, the intelligence quotient (IQ) of children is much lower than that in areas with adequate iodine. 

H. Imura, Inner ring monodeiodination of thyroxine and 3,5,3 -L-triiodothyronine in rat brain. Endocrinology, 109 1619 (1981). 

Triiodothyronine binding in adult rat brain compartmentation of receptor populations in purified neuronal and glial nuclei. Endocrinology, 120 325 (1987). 

J.H. Oppenheimer, H.L Schwartz, and M.I. Surks, Tissue differences in the concentration of triiodothyronine nuclear binding sites in the rat liver, kidney, pituitary, heart, brain, spleen and testis. Endocrinology 95 897 (1974). 

T. Terasaki and W.M. Pardridge, Stereospecificity of triiodothyronine transport into brain, liver and salivary gland role of carrier- and plasma-protein mediated transport. Endocrinology 121 1185-1191 (1987). 

J.H. Oppenheimer and H.L. Schwartz, Stereospecific transport of triiodothyronine from plasma to cytosol and from cytosol to nucleus in rat liver, kidney, brain and heart, J Clin Invest 75 147-154 (1985). 

M.B. Dratman, F.L. Crutchfield, J. Axelrod, R.W. Colburn and T. Nguyen, Localization of triiodothyronine in nerve ending fractions of rat brain, Proc Natl Acad Sci USA 73 941-944 (1976). 

S. Geel. Development-related changes of triiodothyronine binding to brain cytosol receptors. Nature 269 428-430 (1977). 

B. Dozin-Van Roye and Ph. De Nayer. Triiodothyronine binding to brain cytosol receptors during maturation. FEBS Lett. 96 152-154 (1978). 

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