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Anne M Houbrechts, Jolien Van houcke, and Veerle M Darras

gonadosomatic index, altered sex steroid levels and decreased sperm count ( Mukhi & Patino 2007 , Naderi et al. 2014 , Forsatkar et al. 2018 ). Next to systemic TH levels, deiodinases are important players in regulating tissue TH content. By intracellular

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Alvaro Souto Padron, Ruy Andrade Louzada Neto, Thiago Urgal Pantaleão, Maria Carolina de Souza dos Santos, Renata Lopes Araujo, Bruno Moulin de Andrade, Monique da Silva Leandro, João Pedro Saar Werneck de Castro, Andrea Claudia Freitas Ferreira, and Denise Pires de Carvalho

as TSH secretion from rat pituitary fragments, and it was also able to decrease the TSH levels of hypothyroid rats ( Moreno et al . 1998 ). Moreover, 3,5-T2 increases pituitary type 1 iodothyronine deiodinase (D1) activity and transiently decreases

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Aurea Orozco, Carlos Valverde-R, Aurora Olvera, and Carlota García-G

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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Patricia C Lisboa, Ellen P S Conceição, Elaine de Oliveira, and Egberto G Moura

significance in the EO model. The enzyme 5′-iodothyronine deiodinase is responsible for the conversion of T 4 to T 3 . In other words, this enzyme regulates tissue and serum TH availability. Based on some functional criteria, tissue-specific distribution and

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Veerle M Darras and Stijn L J Van Herck

1, type 2 and type 3 iodothyronine deiodinase (D1, D2 and D3). Two of these enzyme types are selective: D2 only catalyses outer ring deiodination (ORD) while D3 only catalyses inner ring deiodination (IRD). The D1 enzyme is non-selective and

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Branka Šošić-Jurjević, Branko Filipović, Kostja Renko, Vladimir Ajdžanović, Milica Manojlović-Stojanoski, Verica Milošević, and Josef Köhrle

Introduction Homeostasis of thyroid hormone (TH) status is regulated by systemic control of TH release from the thyroid and by local enzymatic activation and inactivation of TH in extrathyroidal tissues that is catalyzed by iodothyronine deiodinase

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Type 1 iodothyronine deiodinase in human physiology and disease

Deiodinases: the balance of thyroid hormone

Ana Luiza Maia, Iuri Martin Goemann, Erika L Souza Meyer, and Simone Magagnin Wajner

3 ). In euthyroid individuals, the conversion of peripheral T 4 to T 3 accounts for 80% of all the T 3 produced. This critical step in thyroid hormone metabolism is catalyzed by two enzymes, the type 1 and type 2 iodothyronine deiodinases (D1 and

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Audrey Lamirand, Martine Ramaugé, Michel Pierre, and Françoise Courtin

Introduction Type 2 iodothyronine deiodinase (D2) catalyzes the 5′-deiodination of thyroxine (T 4 ) into the active form of thyroid hormones, 3,5,3′-triiodothyronine (T 3 ; Bianco et al . 2002 , Gereben et al . 2008 ). Notably, in the brain most

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J Kwakkel, H C van Beeren, M T Ackermans, M C Platvoet-ter Schiphorst, E Fliers, W M Wiersinga, and A Boelen

remains unchanged or even decreases. Furthermore, the expression of deiodinating enzymes changes in various tissues ( Wiersinga 2005 ). Deiodinase type 2 (D2; listed as Dio2 in MGI Database) is one of the three known deiodinases. It converts the

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P C Lisboa, E de Oliveira, A C Manhães, A P Santos-Silva, C R Pinheiro, V Younes-Rapozo, L C Faustino, T M Ortiga-Carvalho, and E G Moura

, and T 3 levels have well-known effects on growth and development, thermogenesis, and intermediary metabolism. Two enzyme systems are considered to be markers of thyroid function and reflect the action of TH: 5′-iodothyronine deiodinases and