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PPAR Research
Volume 2016, Article ID 4794576, 17 pages
Review Article

Nutrigenomic Functions of PPARs in Obesogenic Environments

1Department of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE, USA
2Department of Food & Biotechnology, Korea University, Sejong, Republic of Korea
3Department of Food and Nutrition, Seoul Women’s University, Seoul, Republic of Korea
4Department of Food Science and Nutrition, Jeju National University, Jeju, Republic of Korea
5Department of Food and Nutrition and Research Institute of Obesity Science, Sungshin Women’s University, Seoul, Republic of Korea

Received 26 July 2016; Accepted 3 October 2016

Academic Editor: John P. Vanden Heuvel

Copyright © 2016 Soonkyu Chung et al. 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.


Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that mediate the effects of several nutrients or drugs through transcriptional regulation of their target genes in obesogenic environments. This review consists of three parts. First, we summarize current knowledge regarding the role of PPARs in governing the development of white and brown/beige adipocytes from uncommitted progenitor cells. Next, we discuss the interactions of dietary bioactive molecules, such as fatty acids and phytochemicals, with PPARs for the modulation of PPAR-dependent transcriptional activities and metabolic consequences. Lastly, the effects of PPAR polymorphism on obesity and metabolic outcomes are discussed. In this review, we aim to highlight the critical role of PPARs in the modulation of adiposity and subsequent metabolic adaptation in response to dietary challenges and genetic modifications. Understanding the changes in obesogenic environments as a consequence of PPARs/nutrient interactions may help expand the field of individualized nutrition to prevent obesity and obesity-associated metabolic comorbidities.