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  • 1
    Publication Date: 2013-10-29
    Description: Circadian oscillation of body temperature is a basic, evolutionarily conserved feature of mammalian biology. In addition, homeostatic pathways allow organisms to protect their core temperatures in response to cold exposure. However, the mechanism responsible for coordinating daily body temperature rhythm and adaptability to environmental challenges is unknown. Here we show that the nuclear receptor Rev-erbalpha (also known as Nr1d1), a powerful transcriptional repressor, links circadian and thermogenic networks through the regulation of brown adipose tissue (BAT) function. Mice exposed to cold fare considerably better at 05:00 (Zeitgeber time 22) when Rev-erbalpha is barely expressed than at 17:00 (Zeitgeber time 10) when Rev-erbalpha is abundant. Deletion of Rev-erbalpha markedly improves cold tolerance at 17:00, indicating that overcoming Rev-erbalpha-dependent repression is a fundamental feature of the thermogenic response to cold. Physiological induction of uncoupling protein 1 (Ucp1) by cold temperatures is preceded by rapid downregulation of Rev-erbalpha in BAT. Rev-erbalpha represses Ucp1 in a brown-adipose-cell-autonomous manner and BAT Ucp1 levels are high in Rev-erbalpha-null mice, even at thermoneutrality. Genetic loss of Rev-erbalpha also abolishes normal rhythms of body temperature and BAT activity. Thus, Rev-erbalpha acts as a thermogenic focal point required for establishing and maintaining body temperature rhythm in a manner that is adaptable to environmental demands.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839416/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839416/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerhart-Hines, Zachary -- Feng, Dan -- Emmett, Matthew J -- Everett, Logan J -- Loro, Emanuele -- Briggs, Erika R -- Bugge, Anne -- Hou, Catherine -- Ferrara, Christine -- Seale, Patrick -- Pryma, Daniel A -- Khurana, Tejvir S -- Lazar, Mitchell A -- F-32 DK095563/DK/NIDDK NIH HHS/ -- F32 DK095526/DK/NIDDK NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- P30 DK19525/DK/NIDDK NIH HHS/ -- R01 DK045586/DK/NIDDK NIH HHS/ -- R01 DK45586/DK/NIDDK NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- England -- Nature. 2013 Nov 21;503(7476):410-3. doi: 10.1038/nature12642. Epub 2013 Oct 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Department of Genetics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA [2] The Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24162845" target="_blank"〉PubMed〈/a〉
    Keywords: Acclimatization/genetics/physiology ; Adipose Tissue, Brown/metabolism ; Animals ; Body Temperature Regulation/genetics/*physiology ; Circadian Rhythm/genetics/*physiology ; Cold Temperature ; Down-Regulation ; Ion Channels/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondrial Proteins/metabolism ; Nuclear Receptor Subfamily 1, Group D, Member 1/deficiency/genetics/*metabolism ; Thermogenesis/genetics/physiology ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2010-03-05
    Description: The worldwide epidemic of obesity has increased the urgency to develop a deeper understanding of physiological systems related to energy balance and energy storage, including the mechanisms controlling the development of fat cells (adipocytes). The differentiation of committed preadipocytes to adipocytes is controlled by PPARgamma and several other transcription factors, but the molecular basis for preadipocyte determination is not understood. Using a new method for the quantitative analysis of transcriptional components, we identified the zinc-finger protein Zfp423 as a factor enriched in preadipose versus non-preadipose fibroblasts. Ectopic expression of Zfp423 in non-adipogenic NIH 3T3 fibroblasts robustly activates expression of Pparg in undifferentiated cells and permits cells to undergo adipocyte differentiation under permissive conditions. Short hairpin RNA (shRNA)-mediated reduction of Zfp423 expression in 3T3-L1 cells blunts preadipocyte Pparg expression and diminishes the ability of these cells to differentiate. Furthermore, both brown and white adipocyte differentiation is markedly impaired in Zfp423-deficient mouse embryos. Zfp423 regulates Pparg expression, in part, through amplification of the BMP signalling pathway, an effect dependent on the SMAD-binding capacity of Zfp423. This study identifies Zfp423 as a transcriptional regulator of preadipocyte determination.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845731/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845731/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gupta, Rana K -- Arany, Zoltan -- Seale, Patrick -- Mepani, Rina J -- Ye, Li -- Conroe, Heather M -- Roby, Yang A -- Kulaga, Heather -- Reed, Randall R -- Spiegelman, Bruce M -- DK081605/DK/NIDDK NIH HHS/ -- DK31405/DK/NIDDK NIH HHS/ -- F32 DK079507/DK/NIDDK NIH HHS/ -- F32 DK079507-01/DK/NIDDK NIH HHS/ -- F32 DK079507-02/DK/NIDDK NIH HHS/ -- K08 HL79172-01/HL/NHLBI NIH HHS/ -- K99 DK081605/DK/NIDDK NIH HHS/ -- P30 DK040561/DK/NIDDK NIH HHS/ -- P30 DK040561-14/DK/NIDDK NIH HHS/ -- R01 DC008295/DC/NIDCD NIH HHS/ -- R01 DC008295-04/DC/NIDCD NIH HHS/ -- R01DC008295/DC/NIDCD NIH HHS/ -- England -- Nature. 2010 Mar 25;464(7288):619-23. doi: 10.1038/nature08816. Epub 2010 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology and Division of Metabolism and Chronic Disease, Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20200519" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*cytology ; Animals ; *Cell Differentiation ; DNA-Binding Proteins/*metabolism ; Female ; *Gene Expression Regulation, Developmental ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NIH 3T3 Cells ; PPAR gamma/metabolism ; Protein Structure, Tertiary ; Smad Proteins/metabolism ; Transcription Factors/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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