Stéphane MANDARD PhD in Life Sciences / Energy Metabolism

Course and current status

Stéphane Mandard was born in Châteauroux (France). After finishing secondary school, he studied biochemistry for four years before starting in 1997 his university training at the Institute of Biology in Lille where he received his M.S. degree. At this occasion, he explored research within the team of Pr. Dominique Stéhelin, digging into the role of the proto-oncogene c-cbl into thymic apoptosis in mice.

In 1998, after gathering some strong interests in the field of Nuclear Hormone Receptors, he joined the laboratory of Pr Walter Wahli and Pr Béatrice Desvergne (CIG, Université de Lausanne, Switzerland) where he started his Ph.D. project. As part of this study, he worked at deciphering the roles of the nuclear hormone receptors PPAR-alpha and PPAR-beta in energy metabolism.

The Ph.D. degree diploma in one hand, he moved to the Netherlands to work in the team of Pr. Sander Kersten in the Nutrition, Metabolism and Genomics Group, at Wageningen University (Wageningen, The Netherlands). The postdoc project with the title “Determination of the function of the Fasting-induced Adipose Factor FIAF/Angplt4, a direct PPAR target gene” was funded by the Netherlands Organisation for Scientific Research. 

Upon returning to France in September 2005 (laboratory of Pr. Norbert Latruffe), Stéphane is working as an Associate Professor at the University of Bourgogne, in Dijon. His current research focuses on elucidating the role of the peroxisomal 3-ketoacylCoA thiolase B gene in mice, a direct PPAR target gene.

From 2012 onwards, he develops a novel line of research in the team of Dr. Laurent Lagrost, at the INSERM Center (U866) of Dijon. His principal interests revolve around the mechanisms, pathways, and functional implications of bile acids in the detoxification process of bacterial endotoxins (lipopolysaccharides).

University Degrees and Qualification:

2002: PhD in Molecular and Cellular Biology (Lausanne, Switzerland, laboratory of Prof. Walter Wahli and Béatrice Desvergne)

2002-2005: Post-doc fellow (Wageningen, the Netherlands, laboratory of Prof. Sander Kersten)

2005-2011: Associate Professor (University of Burgundy, LBMN Laboratoire de Biochimie Métabolique et Nutritionelle, Inserm Research Center 866 - Lipids, Nutrition, Cancer - Dijon, France, Team Pr Norbert Latruffe).

2012-present: Associate Professor (University of Burgundy, Lipid Transfer Protein and Lipoprotein Metabolism, Inserm Research Center 866 - Lipids, Nutrition, Cancer - Dijon, France, Team Dr Laurent Lagrost, DR1 Inserm).

Member of the editorial board of PPAR Research:


Member of the editorial board of ISRN Hepatology:


Recent publications :

Janssen AW, Houben T, Katiraei S, Dijk W, Boutens L, van der Bolt N, Wang Z, Brown JM, Hazen SL, Mandard S, Shiri-Sverdlov R, Kuipers F, Willems van Dijk K, Vervoort J, Stienstra R, Hooiveld GJ, Kersten S. Modulation of the gut microbiota impacts non-alcoholic fatty liver disease: a potential role for bile acids. J Lipid Res. 2017, doi: 10.1194/jlr.M075713

Saih FE, Andreoletti P, Mandard S, Latruffe N, El Kebbaj MS, Lizard G, Nasser B and Cherkaoui-Malki M, Protective Effect of Cactus Cladode Extracts on Peroxisomal Functions in Microglial BV-2 Cells Activated by Different Lipopolysaccharides. Molecules 2017, 22(1), 102; doi:10.3390/molecules22010102

El Kebbaj R, Andreoletti P, El Hajj HI, El Kharrassi Y, Vamecq J, Mandard S, Saih FE, Latruffe N, El Kebbaj MHS, Lizard G, Nasser B and Cherkaoui-Malki M. Argan oil prevents down-regulation induced by endotoxin on liver fatty acid oxidation and gluconeogenesis and on Peroxisome Proliferator-Activated Receptor Gamma Coactivator-1α, (PGC-1α), Peroxisome Proliferator-Activated Receptor α (PPARα) and Estrogen Related Receptor α (ERRα),2015, Biochimie Open, Vol. 1, p51-59.

V. Aires, B. Brassart, A. Carlier, A. Scagliarini, S. Mandard, E. Limagne, E. Solary, L. Martiny, M. Tarpin and D. Delmas, "A role for Peroxisome Proliferator-Activated Receptor gamma in Resveratrol induced colon cancer cell apoptosis", 2014, Mol Nutr Food Res. 58(9):1785-94. doi: 10.1002/mnfr.201300962. 

V. Nicolas-Francès, S. Arnauld, J. Kaminski, E. ver Loren van Themaat, M.C. Clémencet, J. Chamouton, A. Athias, J. Grober, J. Gresti, P. Degrace, L. Lagrost, N. Latruffe and S. Mandard, "Disturbances in cholesterol, bile acid and glucose metabolism in peroxisomal 3-ketoacylCoA thiolase B deficient mice fed diets containing high or low saturated fat contents", 2014;98:86-101, Biochimie98:86-101. doi: 10.1016/j.biochi.2013.11.014

 A.T. Nguyen, S. Mandard, C. Dray, V. Deckert, P. Vallet, P. Besnard, D.J. Drucker, L. Lagrost and J. Grober "Lipopolysaccharides-mediated increase in glucose-stimulated insulin secretion: Involvement of the glucagon-like peptide 1 (GLP1) pathway", 2014;63(2):471-82, Diabetes. doi: 10.2337/db13-0903

S. Mandard and D. Patsouris: "Nuclear control of the inflammatory response in mammals by Peroxisome Proliferator-Activated Receptors", 2013, PPAR Research.  doi: 10.1155/2013/613864

Reviewers for Biochimie, Amino Acids, Biochemical Pharmacology, Cardiology, Diabetes and Nutrition, Food and Function, Journal of Investigative Dermatology, PPAR Research, Steroids, PLoS One, Annual Research and Review in Biology, Chemical Communication,...

Scientific summary

My former research interests revolved around the mechanisms, pathways, and functional implications of PPARalpha in the control of the expression of FIAF (Fasting Induced Adipose Factor, also known as Angiopoietin-like protein 4 (Angptl4), a pro-hormone released by a variety of different organs and cells types. PPARs are ligand-activated transcription factors that are members of the nuclear hormone receptor superfamily. Three different PPARs are known: PPARα, PPARβ/δ and PPARγ.

Next, I moved towards the field of the peroxisome organelle. At that time, we better characterized the in vitro and in vivo role of the peroxisomal 3-ketoacylCoA thiolase B enzyme (a direct PPAR and HNF4 target gene, Chamouton et al., PPAR Research 2010), which appeared to be critical for the breakdown of very long chain fatty acids.

Partly using transcriptomics, we have been able to provide evidence that besides its catabolic role towards fatty acids, 3-ketoacylCoA thiolase B was also involved in glucose (unpublished data)and cholesterol homeostasis (Fidaleo et al., Biochimie, 2011) as well as in fatty acid content remodeling in liver (Arnauld et al., Biochimie, 2009). To meet these research objectives, functional genomics type of approaches have been followed that combined in vitro studies in hepatic cell lines (HepG2, FAO, H4IIC3,Hepa1.6,….) with experiments in (transgenic) mouse models deficient for the 3-ketoacylCoA thiolase B gene.

From 2012 onwards, I develop a novel line of research in the team of Dr. Laurent Lagrost, at the INSERM Center (U866) of Dijon.

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