Physiol. Genomics Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Physiol. Genomics 38: 54-62, 2009. First published April 21, 2009; doi:10.1152/physiolgenomics.00249.2007
1094-8341/09 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Figures and Tables
Right arrow All Versions of this Article:
38/1/54    most recent
00249.2007v1
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 PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Fromme, T.
Right arrow Articles by Klingenspor, M.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fromme, T.
Right arrow Articles by Klingenspor, M.
Received 23 October 2007; accepted in final form 9 April 2009.
Physiological Genomics 38:54-62 (2009)
1094-8341/09 $8.00 © 2009 American Physiological Society

An intronic single base exchange leads to a brown adipose tissue-specific loss of Ucp3 expression and an altered body mass trajectory

Tobias Fromme 1,2, Christoph Hoffmann 1,2, Kerstin Nau 3, Jan Rozman 1,2, Kathrin Reichwald 4, Michael Utting 4, Matthias Platzer 4 and Martin Klingenspor 1,2

1 Molecular Nutritional Medicine, ZIEL Research Center for Nutrition and Food Sciences, Technische Universität München, Freising
2 Molecular Nutritional Medicine, Else Kröner-Fresenius-Zentrum für Ernährungsmedizin, Technische Universität München, Freising
3 Department of Animal Physiology, Faculty of Biology, Philipps University, Marburg
4 Genome Analysis, Leibniz Institute for Age Research, Fritz Lipmann Institute, Jena, Germany

Uncoupling protein 3 (Ucp3) is a transport protein of the inner mitochondrial membrane and presumably is implicated in the maintenance or tolerance of high lipid oxidation rates. Ucp3 is predominantly expressed in skeletal muscle and brown adipose tissue and is regulated by a transcription factor complex involving peroxisome proliferator-activated receptor-{alpha}, MyoD, and COUP transcription factor II. By analysis of a mutant Djungarian hamster model lacking Ucp3 transcription specifically in brown adipose tissue, we identified a putative transcription factor-binding site that confers tissue specificity. A naturally occurring intronic point mutation disrupting this site leads to brown adipose tissue-specific loss of Ucp3 expression and an altered body weight trajectory. Our findings provide insight into tissue-specific Ucp3 regulation and, for the first time, unambiguously demonstrate that changes in Ucp3 expression can interfere with body weight regulation.

uncoupling protein 3; intronic binding site






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2009 by the American Physiological Society.