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Leptin Raises Defended Body Temperature without Activating Thermogenesis
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. University Medical Center Hamburg-Eppendorf, Germany.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
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Number of Authors: 8
2016 (English)In: Cell reports, ISSN 2211-1247, E-ISSN 2211-1247, Vol. 14, no 7, 1621-1631 p.Article in journal (Refereed) Published
Abstract [en]

Leptin has been believed to exert its weight-reducing action not only by inducing hypophagia but also by increasing energy expenditure/thermogenesis. Leptin-deficient ob/ob mice have correspondingly been thought to be thermogenically limited and to show hypothermia, mainly due to atrophied brown adipose tissue (BAT). In contrast to these established views, we found that BAT is fully functional and that leptin treatment did not increase thermogenesis in wildtype or in ob/ob mice. Rather, ob/ob mice showed a decreased but defended body temperature (i. e., were anapyrexic, not hypothermic) that was normalized to wild-type levels after leptin treatment. This was not accompanied by increased energy expenditure or BAT recruitment but, instead, was mediated by decreased tail heat loss. The weight-reducing hypophagic effects of leptin are, therefore, not augmented through a thermogenic effect of leptin; leptin is, however, pyrexic, i. e., it alters centrally regulated thresholds of thermoregulatory mechanisms, in parallel to effects of other cytokines.

Place, publisher, year, edition, pages
2016. Vol. 14, no 7, 1621-1631 p.
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Biological Sciences
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URN: urn:nbn:se:su:diva-128471DOI: 10.1016/j.celrep.2016.01.041ISI: 000370970200007PubMedID: 26876182OAI: oai:DiVA.org:su-128471DiVA: diva2:915427
Available from: 2016-03-30 Created: 2016-03-29 Last updated: 2016-03-30Bibliographically approved

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Fischer, Alexander W.Abreu-Vieira, Gustavode Jong, Jasper M. A.Petrovic, NatasaCannon, BarbaraNedergaard, Jan
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Department of Molecular Biosciences, The Wenner-Gren Institute
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Cell reports
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