Document Detail


3,5-diiodo-L-thyronine powerfully reduces adiposity in rats by increasing the burning of fats.
MedLine Citation:
PMID:  16014396     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The effect of thyroid hormones on metabolism has long supported their potential as drugs to stimulate fat reduction, but the concomitant induction of a thyrotoxic state has greatly limited their use. Recent evidence suggests that 3,5-diiodo-L-thyronine (T2), a naturally occurring iodothyronine, stimulates metabolic rate via mechanisms involving the mitochondrial apparatus. We examined whether this effect would result in reduced energy storage. Here, we show that T2 administration to rats receiving a high-fat diet (HFD) reduces both adiposity and body weight gain without inducing thyrotoxicity. Rats receiving HFD + T2 showed (when compared with rats receiving HFD alone) a 13% lower body weight, a 42% higher liver fatty acid oxidation rate, appoximately 50% less fat mass, a complete disappearance of fat from the liver, and significant reductions in the serum triglyceride and cholesterol levels (-52% and -18%, respectively). Thyroid hormones and thyroid-stimulating hormone (TSH) serum levels were not influenced by T2 administration. The biochemical mechanism underlying the effects of T2 on liver metabolism involves the carnitine palmitoyl-transferase system and mitochondrial uncoupling. If the results hold true for humans, pharmacological administration of T2 might serve to counteract the problems associated with overweight, such as accumulation of lipids in liver and serum, without inducing thyrotoxicity. However, the results reported here do not exclude deleterious effects of T2 on a longer time scale as well as do not show that T2 acts in the same way in humans.
Authors:
Antonia Lanni; Maria Moreno; Assunta Lombardi; Pieter de Lange; Elena Silvestri; Maurizio Ragni; Paola Farina; Gabriella Chieffi Baccari; Pupah Fallahi; Alessandro Antonelli; Fernando Goglia
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-07-12
Journal Detail:
Title:  FASEB journal : official publication of the Federation of American Societies for Experimental Biology     Volume:  19     ISSN:  1530-6860     ISO Abbreviation:  FASEB J.     Publication Date:  2005 Sep 
Date Detail:
Created Date:  2005-08-29     Completed Date:  2006-03-06     Revised Date:  2012-02-15    
Medline Journal Info:
Nlm Unique ID:  8804484     Medline TA:  FASEB J     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1552-4     Citation Subset:  IM    
Affiliation:
Dipartimento di Scienze della Vita, Seconda Università di Napoli, Caserta, Italy. antonia.lanni@unina2.it
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MeSH Terms
Descriptor/Qualifier:
AMP-Activated Protein Kinases
Adipose Tissue / metabolism*
Adiposity / drug effects*
Animals
Carnitine O-Palmitoyltransferase / metabolism
Cholesterol / blood
Dietary Fats / administration & dosage
Diiodothyronines / pharmacology*,  therapeutic use
Energy Metabolism / drug effects*
Fatty Acids / metabolism
Fatty Liver / drug therapy
Liver / metabolism
Male
Mitochondria, Liver / drug effects,  metabolism
Multienzyme Complexes / metabolism
Oxidation-Reduction
Phosphorylation
Protein-Serine-Threonine Kinases / metabolism
Rats
Rats, Wistar
Triglycerides / blood
Weight Gain / drug effects
Chemical
Reg. No./Substance:
0/Dietary Fats; 0/Diiodothyronines; 0/Fatty Acids; 0/Multienzyme Complexes; 0/Triglycerides; 534-51-0/3,5-diiodothyronine; 57-88-5/Cholesterol; EC 2.3.1.21/Carnitine O-Palmitoyltransferase; EC 2.7.11.1/AMP-Activated Protein Kinases; EC 2.7.11.1/Protein-Serine-Threonine Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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