AJP - Endo AJP: Gastrointestinal and Liver Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Endocrinol Metab 294: E688-E697, 2008. First published February 19, 2008; doi:10.1152/ajpendo.00417.2007
0193-1849/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
294/4/E688    most recent
00417.2007v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Medina-Gomez, G.
Right arrow Articles by Obregon, M.-J.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Medina-Gomez, G.
Right arrow Articles by Obregon, M.-J.

Thermogenic effect of triiodothyroacetic acid at low doses in rat adipose tissue without adverse side effects in the thyroid axis

G. Medina-Gomez, R. M. Calvo,* and M.-J. Obregon*

Instituto de Investigaciones Biomédicas Madrid and Centro de Investigación Biomédica en Red (CIBER) Fisiopatologia Obesidad y Nutricion, Instituto Salud Carlos III, Madrid, Spain

Submitted 2 July 2007 ; accepted in final form 12 February 2008

Triiodothyroacetic acid (TRIAC) is a physiological product of triiodothyronine (T3) metabolism, with high affinity for T3 nuclear receptors. Its interest stems from its potential thermogenic effects. Thus this work aimed 1) to clarify these thermogenic effects mediated by TRIAC vs. T3 in vivo and 2) to determine whether they occurred predominantly in adipose tissues. To examine this, control rats were infused with equimolar T3 or TRIAC doses (0.8 or 4 nmol·100 g body wt–1·day–1) or exposed for 48 h to cold. Both T3 doses and only the highest TRIAC dose inhibited plasma and pituitary thyroid-stimulating hormone (TSH) and thyroxine (T4) in plasma and tissues. Interestingly, the lower TRIAC dose marginally inhibited plasma T4. T3 infusion increased plasma and tissue T3 in a tissue-specific manner. The highest TRIAC dose increased TRIAC concentrations in plasma and tissues, decreasing plasma T3. TRIAC concentrations in tissues were <10% those of T3. Under cold exposure or high T3 doses, TRIAC increased only in white adipose tissue (WAT). Remarkably, only the lower TRIAC dose activated thermogenesis, inducing ectopic uncoupling protein (UCP)-1 expression in WAT and maximal increases in UCP-1, UCP-2, and lipoprotein lipase (LPL) expression in brown adipose tissue (BAT), inhibiting UCP-2 in muscle and LPL in WAT. TRIAC, T3, and cold exposure inhibited leptin secretion and mRNA in WAT. In summary, TRIAC, at low doses, induces thermogenic effects in adipose tissues without concomitant inhibition of TSH or hypothyroxinemia, suggesting a specific role regulating energy balance. This selective effect of TRIAC in adipose tissues might be considered a potential tool to increase energy metabolism.

thermogenesis; leptin; lipoprotein lipase; deiodinases



Address for reprint requests and other correspondence: M.-J. Obregon, Instituto Investigaciones Biomedicas, Arturo Duperier, 4. 28029 Madrid, Spain (e-mail: mjobregon{at}iib.uam.es)







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.