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PPAR Research
Volume 2012 (2012), Article ID 527607, 8 pages
Review Article

Prostaglandins as PPAR Modulators in Adipogenesis

Laboratory of Biodefense and Regulation, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan

Received 29 September 2012; Accepted 20 November 2012

Academic Editor: Shihori Tanabe

Copyright © 2012 Ko Fujimori. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Adipocytes and fat cells play critical roles in the regulation of energy homeostasis. Adipogenesis (adipocyte differentiation) is regulated via a complex process including coordinated changes in hormone sensitivity and gene expression. PPAR is a ligand-dependent transcription factor and important in adipogenesis, as it enhances the expression of numerous adipogenic and lipogenic genes in adipocytes. Prostaglandins (PGs), which are lipid mediators, are associated with the regulation of PPAR function in adipocytes. Prostacyclin promotes the differentiation of adipocyte-precursor cells to adipose cells via activation of the expression of C/EBP and . These proteins are important transcription factors in the activation of the early phase of adipogenesis, and they activate the expression of PPAR , which event precedes the maturation of adipocytes. PGE2 and PGF2α strongly suppress the early phase of adipocyte differentiation by enhancing their own production via receptor-mediated elevation of the expression of cycloxygenase-2, and they also suppress the function of PPAR . In contrast, PGD2 and its non-enzymatic metabolite, - , activate the middle-late phase of adipocyte differentiation through both DP2 receptors and PPAR . This paper focuses on potential roles of PGs as PPAR modulators in adipogenesis and regulators of obesity.