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UCP1 ablation induces obesity and abolishes diet-induced thermogenesis in mice exempt from thermal stress by living at thermoneutrality.
Stockholm University, Faculty of Science, The Wenner-Gren Institute , Physiology.
Stockholm University, Faculty of Science, The Wenner-Gren Institute .
Stockholm University, Faculty of Science, The Wenner-Gren Institute , Physiology.
Stockholm University, Faculty of Science, The Wenner-Gren Institute , Physiology.
2009 (English)In: Cell metabolism, ISSN 1932-7420, Vol. 9, no 2, 203-9 p.Article in journal (Refereed) Published
Abstract [en]

As original studies of UCP1-ablated mice failed to demonstrate an obesogenic effect, alternative mechanisms for adaptive adrenergic thermogenesis have been sought. However, we demonstrate here that in C57Bl6 mice exempt from thermal stress (i.e., kept at thermoneutrality), UCP1 ablation in itself induced obesity, even in mice fed control diet, and vastly augmented diet-induced obesity (high-fat diet); i.e., the mice exhibited increased metabolic efficiency. In wild-type mice, high-fat diet increased norepinephrine-induced thermogenesis; i.e., diet-induced thermogenesis was observed, but no such effect was observed in UCP1-ablated mice, demonstrating that diet-induced thermogenesis fully emanates from UCP1 activity. We conclude that ambient temperature is qualitatively determinative for the outcome of metabolic studies, that no other protein and no other mechanism can substitute for UCP1 in mediating diet-induced adrenergic thermogenesis, and that UCP1 activity can be determinative for obesity development in mice and possibly in humans.

Place, publisher, year, edition, pages
2009. Vol. 9, no 2, 203-9 p.
Keyword [en]
HUMDISEASE
National Category
Physiology
Research subject
Physiology
Identifiers
URN: urn:nbn:se:su:diva-32929DOI: 10.1016/j.cmet.2008.12.014ISI: 000263269400011PubMedID: 19187776OAI: oai:DiVA.org:su-32929DiVA: diva2:281985
Available from: 2009-12-18 Created: 2009-12-18 Last updated: 2011-07-12Bibliographically approved

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