Unbound MEDLINE

A TRbeta selective agonist confers partial resistance to high-fat diet-induced obesity in rats. The Journal of endocrinology [J Endocrinol] Journal article

 
TitleA TRbeta selective agonist confers partial resistance to high-fat diet-induced obesity in rats.
Author(s)Amorim B, Ueta C, Freitas B, Nassif R, Gouveia C, Christoffolete M, Moriscot A, Llimona F, Barbeiro H, Possolo H, Catanozi S, Passareli M, Lancelloti CL, Aoki M, Bianco A, Ribeiro M 
InstitutionB Amorim, Biological Science Course, CCBS,, Presbiterian University Mackenzie, Sao Paulo, Brazil.
SourceJ Endocrinol 2009 Aug 27.
AbstractThyroid hormone receptor beta (TRbeta) 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 TRbeta 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 and adiposity, fasting hyperglycemia and glucose intolerance, increased plasma levels of triglycerides, cholesterol, non-esterified fatty acids and interleukin-6. While GC-24 administration to these animals did not affect food ingestion or modified the progression of body weight 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 TRbeta selective agonist GC-24 only partially improves metabolic control probably as a result of accelerating the resting metabolic rate.
LanguageENG
Pub Type(s)JOURNAL ARTICLE
PubMed ID19713219