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Meyer, C.W.* ; Willershäuser, M.* ; Jastroch, M.* ; Rourke, B.C.* ; Fromme, T.* ; Oelkrug, R.* ; Heldmaier, G.* ; Klingenspor, M.*

Adaptive thermogenesis and thermal conductance in wild-type and UCP1-KO mice.

Am. J. Physiol.-Regul. Integr. Comp. Physiol. 299, R1396-R1406 (2010)
DOI PMC
Open Access Gold as soon as Publ. Version/Full Text is submitted to ZB.
Adaptive thermogenesis and thermal conductance in wild-type and UCP1-KO mice. Am J Physiol Regul Integr Comp Physiol 299: R1396-R1406, 2010. First published September 8, 2010; doi:10.1152/ajpregu.00021.2009.-We compared maximal cold-induced heat production (HPmax) and cold limits between warm (WA; 27 degrees C), moderate cold (MCA; 18 degrees C), or cold acclimated (CA; 5 degrees C) wild-type and uncoupling-protein 1 knockout (UCP1-KO) mice. In wild-type mice, HPmax was successively increased after MCA and CA, and the cold limit was lowered to -8.3 degrees C and -18.0 degrees C, respectively. UCP1-KO mice also increased HPmax in response to MCA and CA, although to a lesser extent. Direct comparison revealed a maximal cold-induced recruitment of heat production by +473 mW and +227 mW in wild-type and UCP1-KO mice, respectively. The increase in cold tolerance of UCP1-KO mice from -0.9 degrees C in MCA to -10.1 degrees C in CA could not be directly related to changes in HPmax, indicating that UCP1-KO mice used the dissipated heat more efficiently than wild-type mice. As judged from respiratory quotients, acutely cold-challenged UCP1-KO mice showed a delayed transition toward lipid oxidation, and 5-h cold exposure revealed diminished physical activity and less variability in the control of metabolic rate. We conclude that BAT is required for maximal adaptive thermogenesis but also allows metabolic flexibility and a rapid switch toward sustained lipid-fuelled thermogenesis as an acute response to cold. In both CA groups, expression of contractile proteins (myosin heavy-chain isoforms) showed minor training effects in skeletal muscles, while cardiac muscle of UCP1-KO mice had novel expression of beta cardiac isoform. Neither respiration nor basal proton conductance of skeletal muscle mitochondria were different between genotypes. In subcutaneous white adipose tissue of UCP1-KO mice, cold exposure increased cytochrome-c oxidase activity and expression of the cell death-inducing DFFA-like effector A by 3.6-fold and 15-fold, respectively, indicating the recruitment of mitochondria-rich brown adipocyte-like cells. Absence of functional BAT leads to remodeling of white adipose tissue, which may significantly contribute to adaptive thermogenesis during cold acclimation.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Nonshivering thermogenesis; cold limit; mitochondrial proton leak; respiratory quotient; myosin heavy chain isoforms
Language english
Publication Year 2010
HGF-reported in Year 2010
ISSN (print) / ISBN 0363-6119
e-ISSN 1522-1490
Journal American Journal of Physiology - Regulatory, Integrative and Comparative Physiology
Quellenangaben Volume: 299, Issue: 5, Pages: R1396-R1406 Article Number: , Supplement: ,
Publisher American Physiological Society
Publishing Place Bethesda
Reviewing status Peer reviewed
Institute(s) Institute of Experimental Genetics (IEG)
Institute of Diabetes and Obesity (IDO)
POF-Topic(s) 30201 - Metabolic Health
Research field(s) Genetics and Epidemiology
PSP Element(s) G-500600-001
PubMed ID 20826705
DOI 10.1152/ajpregu.00021.2009
WOS ID 000283753900031
Scopus ID 78149480633
Erfassungsdatum 2010-12-31
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