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Regulation of FGF21 expression and secretion by retinoic acid receptor-related orphan receptor alpha

Academic Article
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Overview

authors

  • Wang, Y. J.
  • Solt, Laura A.
  • Burris, Thomas

publication date

  • May 2010

journal

  • Journal of Biological Chemistry  Journal

abstract

  • Fibroblast growth factor 21 (FGF21) is a hormone produced by fat and the liver that plays an important role in lipid metabolism. FGF21 expression is induced by peroxisome proliferator-actived receptor alpha in response to physiological conditions requiring increased fatty acid oxidation. Retinoic acid receptor-related receptor alpha (RORalpha) is another nuclear receptor that plays a critical role in lipid metabolism as well as in regulation of the circadian rhythm. In this study we demonstrate that RORalpha directly regulates the expression and secretion of FGF21. A canonical ROR response element was identified in the proximal promoter of the FGF21 gene and shown to exhibit functional activity. Overexpression of RORalpha in HepG2 cells resulted in increased expression and secretion of FGF21. Suppression of RORalpha expression caused a decrease in FGF21 expression and secretion, suggesting that RORalpha contributes to the basal expression of FGF21. These data suggest that one mechanism by which RORalpha regulates lipid metabolism may be by modulation of FGF21 secretion. Furthermore, this study identifies a clear link between RORalpha, a key regulator of the mammalian clock, and FGF21, an important hormone regulating glucose and lipid homeostasis.

subject areas

  • Animals
  • Circadian Rhythm
  • Fibroblast Growth Factors
  • Gene Expression Regulation
  • Glucose
  • Hep G2 Cells
  • Homeostasis
  • Humans
  • Lipid Metabolism
  • Mice
  • Nuclear Receptor Subfamily 1, Group F, Member 1
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Identity

PubMed Central ID

  • PMC2871432

International Standard Serial Number (ISSN)

  • 0021-9258

Digital Object Identifier (DOI)

  • 10.1074/jbc.M110.102160

PubMed ID

  • 20332535
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Additional Document Info

start page

  • 15668

end page

  • 15673

volume

  • 285

issue

  • 21

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