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Caveolin-1-ablated mice survive in cold by nonshivering thermogenesis despite desensitized adrenergic responsiveness
Stockholm University, Faculty of Science, The Wenner-Gren Institute , Physiology.
Stockholm University, Faculty of Science, The Wenner-Gren Institute , Physiology.
Stockholm University, Faculty of Science, The Wenner-Gren Institute , Physiology.
Stockholm University, Faculty of Science, The Wenner-Gren Institute , Physiology.
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2010 (English)In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 299, no 3, E374-83 p.Article in journal (Refereed) Published
Abstract [en]

Caveolin-1 (Cav1)-ablated mice display impaired lipolysis in white adipose tissue. They also seem to have an impairment in brown adipose tissue function, implying that Cav1-ablated mice could encounter problems in surviving longer periods in cold temperatures. To investigate this, Cav1-ablated mice and wild-type mice were transferred to cold temperatures for extended periods of time, and parameters related to metabolism and thermogenesis were investigated. Unexpectedly, the Cav1-ablated mice survived in the cold. There were no differences between Cav1-ablated and wild-type mice with regard to food intake, in behavior related to shivering, or in body temperature. The Cav1-ablated mice had a halved total fat content independently of acclimation temperature. There was no difference in brown adipose tissue uncoupling protein-1 (UCP1) protein amount, and isolated brown fat mitochondria were thermogenically competent but displayed 30% higher thermogenic capacity. However, the beta(3)-adrenergic receptor amount was reduced by about one-third in the Cav1-ablated mice at all acclimation temperatures. Principally in accordance with this, a higher than standard dose of norepinephrine was needed to obtain full norepinephrine-induced thermogenesis in the Cav1-ablated mice; the higher dose was also needed for the Cav1-ablated mice to be able to utilize fat as a substrate for thermogenesis. In conclusion, the ablation of Cav1 impairs brown adipose tissue function by a desensitization of the adrenergic response; however, the desensitization is not evident in the animal as it is overcome physiologically, and Cav1-ablated mice can therefore survive in prolonged cold by nonshivering thermogenesis.

Place, publisher, year, edition, pages
2010. Vol. 299, no 3, E374-83 p.
Keyword [en]
brown adipose tissue; norepinephrine; brown fat mitochondria; respiratory quotient
National Category
Cell and Molecular Biology
Research subject
Physiology
Identifiers
URN: urn:nbn:se:su:diva-45247DOI: 10.1152/ajpendo.00071.2010ISI: 000281260500005PubMedID: 20530737OAI: oai:DiVA.org:su-45247DiVA: diva2:368238
Available from: 2010-11-09 Created: 2010-11-09 Last updated: 2017-12-12Bibliographically approved

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Csikasz, Robert IShabalina, Irina GNedergaard, JanCannon, Barbara
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