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Physiol. Genomics (October 11, 2005). doi:10.1152/physiolgenomics.00204.2005
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Submitted on August 11, 2005
Accepted on October 9, 2005

EVIDENCE FOR NR4A1 AS A COLD-INDUCED EFFECTOR OF BROWN FAT THERMOGENESIS

Timo Kanzleiter1, Tatjana Schneider1, Isabel Walter1, Florian Bolze1, Christoph Eickhorst1, Gerhard Heldmaier1, Susanne Klaus2, and Martin Klingenspor1*

1 Department of Animal Physiology, Philipps-University Marburg, Biology Faculty, Marburg, Hessen, Germany
2 German Institute of Human Nutrition in Potsdam, Nuthetal, Germany

* To whom correspondence should be addressed. E-mail: klingens{at}staff.uni-marburg.de.

Acute cold exposure leads to noradrenaline release in brown adipose tissue (BAT) and activates UCP1-mediated non-shivering thermogenesis. Chronic sympathetic stimulation is known to initiate mitochondrial biogenesis, UCP1 expression, hyperplasia of BAT and recruitment of brown adipocytes in white adipose tissue (WAT) depots. Despite distinct functions of BAT and WAT in energy balance only a few genes are exclusively expressed in either tissue. We identified NUR77 (Nr4a1), an orphan receptor, to be induced transiently in brown adipocytes in response to {beta}-adrenergic stimulation and in BAT of cold exposed mice. Subsequent reporter gene assays demonstrated an inhibitory action of NUR77 on basal and PPAR{gamma}/RXR{alpha} mediated transactivation of the Ucp1 enhancer in heterologous cotransfection experiments. Despite this function of NUR77 in the control of Ucp1 gene expression, non-shivering thermogenesis was not affected in Nur77-knockout mice. However, we observed a superinduction of Nor1 in BAT of cold exposed knockout mice. We conclude that NUR77 is a coldinduced negative regulator of Ucp1, but phenotypic consequences in knockout mice are compensated by functional redundancy of Nor1.




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