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iodothyronine deiodinases (Ds). Indeed, iodothyronine deiodination is the essential first step in the pre-receptor control mechanism of TH action ( Nobel et al . 2001 ). From an evolutionary perspective, Ds may be considered pivotal players in the emergence and
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specific receptors in the arcuate nucleus of the hypothalamus, induce neuroendocrine changes resulting in increased release of TRH from the hypothalamus, TSH from the pituitary gland, and thereby TH from the thyroid glands ( Costa da Veiga et al . 2004
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adrenergic receptors and protein synthesis. Thyroid hormones affect excitation/contractility coupling and have inotropic properties ( Ririe et al . 1995 ), which are dose-dependent ( Snow et al . 1992 ), and are strong vasodilators of systemic arteries
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). Indeed, as discussed in detail below, direct SCN projections target many of the key neurosecretory hypothalamic cell groups including corticotrophin releasing hormone (CRH), thyrotrophin-releasing hormone (TRH), gonadotrophin-releasing hormone (GnRH) and
Type 1 iodothyronine deiodinase in human physiology and disease
Deiodinases: the balance of thyroid hormone
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. 1998 ). In addition, the human DIO1 promoter contains thyroid hormone response-retinoic acid (RA) response elements that mediate thyroid hormone receptor (TR)β activation ( Schreck et al . 1994 , Toyoda et al . 1995 ). Interestingly, a recent
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Department of Physiological Sciences, Department of Basic and Experimental Nutrition, Laboratory of Molecular Endocrinology, Department of Applied Nutrition, Roberto Alcântara Gomes Biology Institute
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with multiple unrelated targets including receptors, enzymes, ion channels, and transporters ( Beher et al . 2009 , Pacholec et al . 2010 ). It seems that to decrease lipid peroxidation, Res has to be acting in an animal with some increased level of
DZHK (German Center for Cardiovascular Research), Partner Site Greifswald, Greifswald, Germany
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(the hypothalamic–pituitary–thyroid (HPT) axis). An increase in circulating thyroid hormones (THs) in turn causes suppression of synthesis and release of both TRH and TSH, which in turn suppress TH secretion from the thyroid. Due to their highly
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al. 2015 , Cubuk et al. 2017 a ). However, many other components like deiodinase enzymes, transporters and receptors are involved in T3 availability in the brain and require much more detailed analysis over the course of a torpor bout (Fig. 5
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release after TRH in aging male and female rats . Endocrine Research Communications 9 169 – 177 . ( doi:10.3109/07435808209045762 ) Grossman W 1980 Cardiac hypertrophy: useful adaptation or pathologic process? American Journal of Medicine
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other secretagogs, e.g. thyroptropin-releasing hormone (TRH), GHRH, and gonadotropin-releasing hormone (GnRH), evoked no adenohypophyseal hormone secretion ( Meij et al. 1997 d ). Eight weeks after surgery, the CRH stimulation test was not able to