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PPARγ Modulates Long Chain Fatty Acid Processing in the Intestinal Epithelium

Lee Kong Chian School of Medicine, Nanyang Technological University, 11 Mandalay Road, Singapore 308232, Singapore
Center for Integrative Genomics, University of Lausanne, Génopode, CH-1015 Lausanne, Switzerland
Department of Nutritional Sciences, University of Vienna, Althanstrasse 14, 1090 Vienna,Austria
Turku Centre for Biotechnology, University of Turku and Åbo Akademi University,Tykisokatu 6, 20520 Turku, Finland
Institut du Thorax, INSERM, CNRS, UNIV Nantes, 44007 Nantes, France
Vienna Metabolomics Center (VIME), University of Vienna, Althanstrasse 14, 1090 Vienna, Austria
ToxAlim, Research Center in Food Toxicology, National Institute for Agricultural Research (INRA),180 Chemin de Tournefeuille, 31300 Toulouse, France
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2017, 18(12), 2559;
Received: 7 November 2017 / Revised: 24 November 2017 / Accepted: 27 November 2017 / Published: 28 November 2017
(This article belongs to the Special Issue PPARs in Cellular and Whole Body Energy Metabolism)
PDF [3336 KB, uploaded 28 November 2017]


Nuclear receptor PPARγ affects lipid metabolism in several tissues, but its role in intestinal lipid metabolism has not been explored. As alterations have been observed in the plasma lipid profile of ad libitum fed intestinal epithelium-specific PPARγ knockout mice (iePPARγKO), we submitted these mice to lipid gavage challenges. Within hours after gavage with long chain unsaturated fatty acid (FA)-rich canola oil, the iePPARγKO mice had higher plasma free FA levels and lower gastric inhibitory polypeptide levels than their wild-type (WT) littermates, and altered expression of incretin genes and lipid metabolism-associated genes in the intestinal epithelium. Gavage with the medium chain saturated FA-rich coconut oil did not result in differences between the two genotypes. Furthermore, the iePPARγKO mice did not exhibit defective lipid uptake and stomach emptying; however, their intestinal transit was more rapid than in WT mice. When fed a canola oil-rich diet for 4.5 months, iePPARγKO mice had higher body lean mass than the WT mice. We conclude that intestinal epithelium PPARγ is activated preferentially by long chain unsaturated FAs compared to medium chain saturated FAs. Furthermore, we hypothesize that the iePPARγKO phenotype originates from altered lipid metabolism and release in epithelial cells, as well as changes in intestinal motility. View Full-Text
Keywords: PPARγ; intestine; lipid metabolism PPARγ; intestine; lipid metabolism

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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 (CC BY 4.0).

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Duszka, K.; Oresic, M.; Le May, C.; König, J.; Wahli, W. PPARγ Modulates Long Chain Fatty Acid Processing in the Intestinal Epithelium. Int. J. Mol. Sci. 2017, 18, 2559.

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