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Journal of Endocrinology (2009) 203, 291-299       DOI: 10.1677/JOE-08-0539
© 2009 Society for Endocrinology
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A TRβ-selective agonist confers resistance to diet-induced obesity

 Beatriz S Amorim1,3,*, Cintia B Ueta1,3,*, Beatriz C G Freitas2, Renata J Nassif1, Cecília Helena de Azevedo Gouveia3, Marcelo A Christoffolete4, Anselmo S Moriscot4, Carmen Lucia Lancelloti8, Flávia Llimona6, Hermes Vieira Barbeiro6, Heraldo Possolo de Souza6, Sergio Catanozi5, Marisa Passarelli5, Marcelo S Aoki7, Antonio C Bianco2 and Miriam O Ribeiro1

1 Biological Science Course, CCBS, Presbyterian University Mackenzie, Rua da Consolação, 930 Prédio 38, Curso de Biologia, São Paulo, SP 01302-907, Brazil
2 Division of Endocrinology, Diabetes and Metabolism, University of Miami Miller School of Medicine, Miami, Florida 33136, USA
3 Department of Anatomy, Institute of Biomedical Sciences
4 Department of Cell and Developmental Biology, Institute of Biomedical Sciences
5 Lipids Laboratory (LIM 10) Faculty of Medical Sciences
6 Clinical Emergency, Faculty of Medical Sciences
7 School of Arts, Sciences and Humanities, University of São Paulo, São Paulo, SP, Brazil
8 AFIP and Pathology, School of Medical Sciences, Santa Casa, São Paulo 04020-060, SP, Brazil

(Correspondence should be addressed to M O Ribeiro; Email: miriamribeiro{at}mackenzie.br)

* (B S Amorim and C B Ueta contributed equally to this work)

Thyroid hormone receptor β (TRβ also listed as THRB on the MGI Database)-selective agonists activate brown adipose tissue (BAT) thermogenesis, while only minimally affecting cardiac activity or lean body mass. Here, we tested the hypothesis that daily administration of the TRβ agonist GC-24 prevents the metabolic alterations associated with a hypercaloric diet. Rats were placed on a high-fat diet and after a month exhibited increased body weight (BW) and adiposity, fasting hyperglycemia and glucose intolerance, increased plasma levels of triglycerides, cholesterol, nonesterified fatty acids and interleukin-6. While GC-24 administration to these animals did not affect food ingestion or modified the progression of BW gain, it did increase energy expenditure, eliminating the increase in adiposity without causing cardiac hypertrophy. Fasting hyperglycemia remained unchanged, but treatment with GC-24 improved glucose tolerance by increasing insulin sensitivity, and also normalized plasma triglyceride levels. Plasma cholesterol levels were only partially normalized and liver cholesterol content remained high in the GC-24-treated animals. Gene expression in liver, skeletal muscle, and white adipose tissue was only minimally affected by treatment with GC-24, with the main target being BAT. In conclusion, during high-fat feeding treatment with the TRβ-selective agonist, GC-24 only partially improves metabolic control probably as a result of accelerating the resting metabolic rate.






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