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Thyroid hormone central regulation

In addition to the obvious deactivating role of deiodinases, there has been recent evidence that a relationship exists between regulation of deiodination of thyroid hormones in target cells and the intracellular effects of T4 and T3 on pituitary and hypothalamus function. In the rat pituitary, and probably the human, type-II deiodinase-catalyzed conversion of T4 to T3 is a prerequisite for inhibition of TRH release. rT3, produced from T4 by type-III deiodinase, is a potent inhibitor of type-II deiodinase. In a postulated regulatory circuit, rT3 formed from T4 by type-III deiodinase in surrounding CNS (Central Nervous System) tissue enters the pituitary and inhibits type-II enzyme. The resulting decrease in T3 concentration, in turn, causes an increase in TSH secretion49. [Pg.1503]

It is assumed that some compounds of this group (AHTN and ATTN) may bind to the retinoid acid receptor (RAR) or retinoid X receptor (RXR) because their structure shows some similarity with synthetic RXR ligands [364,365]. The RAR and RXR belong to the steroid/thyroid hormone nuclear receptor super family. They play a central role in the regulation of many intracellular receptor pathways [366]. However, all these assumptions and predictions, especially the predicted high bioconcentration potential of the PMFs, have to be investigated experimentally. [Pg.137]

The next set of issues on the detected iriRNAs utilizing the hyt/hvt mice were l)To identify brain and cer ral cortex iriRNAs possibly regulated by thyroid hormone in fetal and neonatal brain and 2)To try to determine vhy some iriRNAs were specifically altered. To do this, zeta probe eets for northern gel hybridizations were prepared from 1, 5 and 7 day central cortex, brain remainder, and total brain RNA from hyt/hyt and hyt/+ littermates. These sheets were hybridized to cDNA probes reflecting iriRNAs that had been detected in cerebral cortex and total brain (Figures 4 and 5). [Pg.67]

Thyroliberin, thyrotropin-releasing hormone, TRH, pGlu-His-Pro-NH2, produced in the paraventricular nucleus of the hypothalamus, stimulates biosynthesis and secretion of thyrotropin (TSH) from the anterior pituitary. It is central in regulating the hypothalamic-pituitary-thyroid (HPT) axis. Furthermore, TRH influences the release of other hormones, e.g., prolactin, growth hormone, vasopressin, insulin, and also the classic neurotransmitters norepinephrine (noradrenaline) and epinephrine (adrenaline). In addition, it is... [Pg.374]


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