Horm Metab Res 2006; 38(8): 481-485
DOI: 10.1055/s-2006-949527
Original Basic

© Georg Thieme Verlag KG Stuttgart · New York

Leptin Acute Modulation of the 5′-deiodinase Activities in Hypothalamus, Pituitary and Brown Adipose Tissue of Fed Rats

A. Cabanelas 1 , P. C. Lisboa 2 , E. G. Moura 2 , C. C. Pazos-Moura 1
  • 1Laboratório de Endocrinologia Molecular, Instituto de Biofísica Carlos Chagas Filho, UFRJ, CCS, Bloco G, Cidade Universitária, Rio de Janeiro, RJ, Brazil
  • 2Laboratório de Fisiologia Endócrina, Departamento de Ciências Fisiológicas, Instituto de Biologia Roberto Alcântara Gomes, UERJ, Rio de Janeiro, RJ, Brazil
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Publikationsverlauf

Received 24 November 2005

Accepted after revision 14 February 2006

Publikationsdatum:
29. August 2006 (online)

Abstract

Leptin and thyroid hormones (TH) have the ability to increase energy expenditure. Biological effects of TH are dependent on thyroxine (T4) to triiodothyronine (T3) conversion by deiodinase type 1 (D1) and type 2 (D2). Leptin has been shown to stimulate the hypothalamus-pituitary-thyroid axis and, also, to modulate 5′-deiodinases in different tissues, depending on energetic status of animals. Here, we examined the acute effects of leptin on hypothalamic, pituitary and BAT D2 and pituitary D1 activities. Male fed rats received a single subcutaneous injection of saline or leptin (8 μg/100 g BW) and sacrificed 2 hours later. Leptin promoted an important decrease in hypothalamic D2 (55% reduction, p <0.001) with no changes in pituitary D2, in concomitance with a 2-fold rise in serum TSH, suggesting that leptin acted at hypothalamus in order to stimulate TRH-TSH axis. In addition, BAT D2 was decreased by 25% (p<0.05). In contrast, pituitary D1 showed a 2-fold increase (p<0.001), indicating that, as demonstrated before for liver and thyroid D1, the pituitary enzyme is also acutely up-regulated by leptin. Serum concentrations of insulin and TH of leptin-injected animals remained unchanged. Regulation of 5′-deiodinases directing the local T3 production, is a mechanism by which leptin may alter hypothalamic, pituitary and BAT functions.

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Correspondence

Carmen C. Pazos de Moura

Laboratório de Endocrinologia Molecular·Instituto de Biofísica Carlos Chagas Filho·UFRJ, CCS, Bloco G·Cidade Universitária

Ilha do Fundão·CEP 21949·900·Rio de Janeiro, RJ·Brazil

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