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PPARalpha does not suppress muscle-associated gene expression in brown adipocytes but does influence expression of factors that fingerprint the brown adipocyte.
Stockholms universitet, Naturvetenskapliga fakulteten, Wenner-Grens institut.
Stockholms universitet, Naturvetenskapliga fakulteten, Wenner-Grens institut.
Stockholms universitet, Naturvetenskapliga fakulteten, Wenner-Grens institut.ORCID-id: 0000-0003-2070-1587
2010 (engelsk)Inngår i: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 397, nr 2, s. 146-51Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Brown adipocytes and myocytes develop from a common adipomyocyte precursor. PPARalpha is a nuclear receptor important for lipid and glucose metabolism. It has been suggested that in brown adipose tissue, PPARalpha represses the expression of muscle-associated genes, in this way potentially acting to determine cell fate in brown adipocytes. To further understand the possible role of PPARalpha in these processes, we measured expression of muscle-associated genes in brown adipose tissue and brown adipocytes from PPARalpha-ablated mice, including structural genes (Mylpf, Tpm2, Myl3 and MyHC), regulatory genes (myogenin, Myf5 and MyoD) and a myomir (miR-206). However, in our hands, the expression of these genes was not influenced by the presence or absence of PPARalpha, nor by the PPARalpha activator Wy-14,643. Similarly, the expression of genes common for mature brown adipocyte and myocytes (Tbx15, Meox2) were not affected. However, the brown adipocyte-specific regulatory genes Zic1, Lhx8 and Prdm16 were affected by PPARalpha. Thus, it would not seem that PPARalpha represses muscle-associated genes, but PPARalpha may still play a role in the regulation of the bifurcation of the adipomyocyte precursor into a brown adipocyte or myocyte phenotype.

sted, utgiver, år, opplag, sider
2010. Vol. 397, nr 2, s. 146-51
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URN: urn:nbn:se:su:diva-45267DOI: 10.1016/j.bbrc.2010.05.053ISI: 000279718900005PubMedID: 20471959OAI: oai:DiVA.org:su-45267DiVA, id: diva2:369183
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authorCount :3Tilgjengelig fra: 2010-11-10 Laget: 2010-11-10 Sist oppdatert: 2022-02-24bibliografisk kontrollert

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