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PPARγ Modulates Long Chain Fatty Acid Processing in the Intestinal Epithelium
Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore; Center for Integrative Genomics, University of Lausanne, Génopode, Lausanne, Switzerland; Department of Nutritional Sciences, University of Vienna, Vienna, Austria.
Turku Centre for Biotechnology, University of Turku and Åbo Akademi University,Turku, Finland.ORCID iD: 0000-0002-2856-9165
Institut du Thorax, INSERM, CNRS, UNIV Nantes, Nantes, France.
Department of Nutritional Sciences, University of Vienna, Vienna, Austria; Vienna Metabolomics Center (VIME), University of Vienna, Vienna, Austria.
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2017 (English)In: International Journal of Molecular Sciences, ISSN 1422-0067, E-ISSN 1422-0067, Vol. 18, no 12, E2559Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
Basel, Switzerland: MDPI , 2017. Vol. 18, no 12, E2559
Keyword [en]
PPARγ, intestine, lipid metabolism
National Category
Medical and Health Sciences Biochemistry and Molecular Biology
Identifiers
URN: urn:nbn:se:oru:diva-63724DOI: 10.3390/ijms18122559ISI: 000418896700063PubMedID: 29182565Scopus ID: 2-s2.0-85036561612OAI: oai:DiVA.org:oru-63724DiVA: diva2:1169311
Funder
EU, FP7, Seventh Framework Programme
Note

Funding Agencies:

Swiss National Science Foundation

Bonizzi-Theler-Stiftung

Etat de Vaud 

Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore

Available from: 2017-12-23 Created: 2017-12-23 Last updated: 2018-01-19Bibliographically approved

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Oresic, Matej

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