8
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Retinoid-related orphan receptor alpha and the regulation of lipid homeostasis.

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Many nuclear hormone receptors (NRs) control lipid, glucose and energy homeostasis in an organ specific manner. Concordantly, dysfunctional NR signalling results in metabolic disease. The Retinoic acid receptor-related orphan receptor alpha (RORα), a member of the NR1F subgroup, is expressed in metabolic tissues. Previous studies identified the role of this NR in dyslipidemia, apo-lipoprotein metabolism and atherosclerosis. Recent data is underscoring the significant role of this orphan NR in the regulation of phase I/II metabolism (bile acids, xenobiotics, steroids etc.), adiposity, insulin signalling, and glucose tolerance. Moreover, oxygenated sterols, have been demonstrated to function as native ligands and inverse agonists. This review focuses on the rapidly emerging and evolving role of RORα in the control of lipid and glucose homeostasis in major mass metabolic tissues. Article from the special issue orphan receptors.

          Related collections

          Author and article information

          Journal
          J. Steroid Biochem. Mol. Biol.
          The Journal of steroid biochemistry and molecular biology
          1879-1220
          0960-0760
          Jul 2012
          : 130
          : 3-5
          Affiliations
          [1 ] Obesity Research Centre, Institute for Molecular Bioscience, University of Queensland, Services Rd St. Lucia, Queensland, 4072 Australia.
          Article
          S0960-0760(11)00132-4
          10.1016/j.jsbmb.2011.06.009
          21723946
          96cd405e-9963-41b1-9f02-616488ca1ee5
          Copyright © 2011 Elsevier Ltd. All rights reserved.
          History

          Comments

          Comment on this article