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Oelkrug, R.* ; Heldmaier, G.* ; Meyer, C.W.*

Torpor patterns, arousal rates, and temporal organization of torpor entry in wildtype and UCP1-ablated mice.

J. Comp. Physiol. B 181, 137-45 (2011)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
In eutherian mammals, uncoupling protein 1 (UCP1) mediated non-shivering thermogenesis from brown adipose tissue (BAT) provides a mechanism through which arousal from torpor and hibernation is facilitated. In order to directly assess the magnitude by which the presence or absence of UCP1 affects torpor patterns, rewarming and arousal rates within one species we compared fasting induced torpor in wildtype (UCP1(+/+)) and UCP1-ablated mice (UCP(-/-)). Torpor was induced by depriving mice of food for up to 48 h and by a reduction of ambient temperature (T (a)) from 30 to 18°C at four different time points after 18, 24, 30 and 36 h of food deprivation. In most cases, torpor bouts occurred within 20 min after the switch in ambient temperature (30-18°C). Torpor bouts expressed during the light phase lasted 3-6 h while significantly longer bouts (up to 16 h) were observed when mice entered torpor during the dark phase. The degree of hypometabolism (5-22 ml h(-1)) and hypothermia (19.5-26.7°C) was comparable in wildtype and UCP1-ablated mice, and both genotypes were able to regain normothermia. In contrast to wildtype mice, UCP1-ablated mice did not display multiple torpor bouts per day and their peak rewarming rates from torpor were reduced by 50% (UCP1(+/+): 0.24 ± 0.08°C min(-1); UCP1(-/-): 0.12 ± 0.04°C min(-1)). UCP1-ablated mice therefore took significantly longer to rewarm from 25 to 32°C (39 vs. 70 min) and required 60% more energy for this process. Our results demonstrate the energetic benefit of functional BAT for rapid arousal from torpor. They also suggest that torpor entry and maintenance may be dependent on endogenous rhythms.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 2011
HGF-Berichtsjahr 0
ISSN (print) / ISBN 0174-1578
e-ISSN 1432-136X
Quellenangaben Band: 181, Heft: 1, Seiten: 137-45 Artikelnummer: , Supplement: ,
Verlag Springer
Begutachtungsstatus Peer reviewed
PubMed ID 20680295
Erfassungsdatum 2011-12-31