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1. Lipo-chitooligosaccharides as regulatory signals of fungal growth and development

Author

Tomás Allen Rush, Virginie Puech-Pagès, Adeline Bascaules, Patricia Jargeat, Fabienne Maillet, Alexandra Haouy, Arthur QuyManh Maës, Cristobal Carrera Carriel, Devanshi Khokhani, Michelle Keller-Pearson, Joanna Tannous, Kevin R. Cope, Kevin Garcia, Junko Maeda, Chad Johnson, Bailey Kleven, Quanita J. Choudhury, Jessy Labbé, Candice Swift, Michelle A. O’Malley, Jin Woo Bok, Sylvain Cottaz, Sébastien Fort, Verena Poinsot, Michael R. Sussman, Corinne Lefort, Jeniel Nett, Nancy P. Keller, Guillaume Bécard, and Jean-Michel Ané

Subjects
Science
Abstract

Lipo-chitooligosaccharides (LCOs) are signaling molecules produced by certain bacteria and fungi that establish symbiotic relationships with plants. Here, the authors show that LCOs are produced also by many other, non-symbiotic fungi, and regulate fungal growth and development.

Published
2020
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2. Natriuretic peptides promote glucose uptake in a cGMP-dependent manner in human adipocytes

Author

Marine Coué, Valentin Barquissau, Pauline Morigny, Katie Louche, Corinne Lefort, Aline Mairal, Christian Carpéné, Nathalie Viguerie, Peter Arner, Dominique Langin, Mikael Rydén, and Cedric Moro

Subjects
Medicine, Science
Abstract

Abstract Robust associations between low plasma level of natriuretic peptides (NP) and increased risk of type 2 diabetes (T2D) have been recently reported in humans. Adipose tissue (AT) is a known target of NP. However it is unknown whether NP signalling in human AT relates to insulin sensitivity and modulates glucose metabolism. We here show in two European cohorts that the NP receptor guanylyl cyclase-A (GC-A) expression in subcutaneous AT was down-regulated as a function of obesity grade while adipose NP clearance receptor (NPRC) was up-regulated. Adipose GC-A mRNA level was down-regulated in prediabetes and T2D, and negatively correlated with HOMA-IR and fasting blood glucose. We show for the first time that NP promote glucose uptake in a dose-dependent manner. This effect is reduced in adipocytes of obese individuals. NP activate mammalian target of rapamycin complex 1/2 (mTORC1/2) and Akt signalling. These effects were totally abrogated by inhibition of cGMP-dependent protein kinase and mTORC1/2 by rapamycin. We further show that NP treatment favoured glucose oxidation and de novo lipogenesis independently of significant gene regulation. Collectively, our data support a role for NP in blood glucose control and insulin sensitivity by increasing glucose uptake in human adipocytes. This effect is partly blunted in obesity.

Published
2018
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3. Immune Cell Toll-like Receptor 4 Mediates the Development of Obesity- and Endotoxemia-Associated Adipose Tissue Fibrosis

Author

Isabelle K. Vila, Pierre-Marie Badin, Marie-Adeline Marques, Laurent Monbrun, Corinne Lefort, Lucile Mir, Katie Louche, Virginie Bourlier, Balbine Roussel, Philippe Gui, Jacques Grober, Vladimír Štich, Lenka Rossmeislová, Alexia Zakaroff-Girard, Anne Bouloumié, Nathalie Viguerie, Cedric Moro, Geneviève Tavernier, and Dominique Langin

Subjects
Biology (General), QH301-705.5
Abstract

Adipose tissue fibrosis development blocks adipocyte hypertrophy and favors ectopic lipid accumulation. Here, we show that adipose tissue fibrosis is associated with obesity and insulin resistance in humans and mice. Kinetic studies in C3H mice fed a high-fat diet show activation of macrophages and progression of fibrosis along with adipocyte metabolic dysfunction and death. Adipose tissue fibrosis is attenuated by macrophage depletion. Impairment of Toll-like receptor 4 signaling protects mice from obesity-induced fibrosis. The presence of a functional Toll-like receptor 4 on adipose tissue hematopoietic cells is necessary for the initiation of adipose tissue fibrosis. Continuous low-dose infusion of the Toll-like receptor 4 ligand, lipopolysaccharide, promotes adipose tissue fibrosis. Ex vivo, lipopolysaccharide-mediated induction of fibrosis is prevented by antibodies against the profibrotic factor TGFβ1. Together, these results indicate that obesity and endotoxemia favor the development of adipose tissue fibrosis, a condition associated with insulin resistance, through immune cell Toll-like receptor 4.

Published
2014
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4. Lipo-chitooligosaccharides as regulatory signals of fungal growth and development

Author

Candice L. Swift, Arthur QuyManh Maes, Nancy P. Keller, Cristobal Carrera Carriel, Kevin Garcia, Guillaume Bécard, Joanna Tannous, Quanita J. Choudhury, Jean-Michel Ané, Michelle A. O’Malley, Junko Maeda, Jin Woo Bok, Michelle Keller-Pearson, Tomás Allen Rush, Patricia Jargeat, Virginie Puech-Pagès, Sylvain Cottaz, Michael R. Sussman, Fabienne Maillet, Jeniel E. Nett, Adeline Bascaules, Jessy Labbé, Kevin R. Cope, Alexandra Haouy, Bailey Kleven, Véréna Poinsot, Chad J. Johnson, Sébastien Fort, Corinne Lefort, Devanshi Khokhani, Fort, Sébastien, University of Wisconsin-Madison, Oak Ridge National Laboratory [Oak Ridge] (ORNL), UT-Battelle, LLC, Evolution des Interactions Plantes-Microorganismes, Laboratoire de Recherche en Sciences Végétales (LRSV), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Metatoul - Agromix, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-MetaboHUB-MetaToul, Génopole Toulouse Midi-Pyrénées [Auzeville] (GENOTOUL), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Génopole Toulouse Midi-Pyrénées [Auzeville] (GENOTOUL), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Interactions moléculaires et réactivité chimique et photochimique (IMRCP), Institut de Chimie de Toulouse (ICT-FR 2599), Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Evolution et Diversité Biologique (EDB), Laboratoire des Interactions Plantes Microbes Environnement (LIPME), Centre National de la Recherche Scientifique (CNRS)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), South Dakota State University (SDSTATE), North Carolina State University [Raleigh] (NC State), University of North Carolina System (UNC), The University of Tennessee [Knoxville], University of Georgia [USA], University of California [Santa Barbara] (UC Santa Barbara), University of California (UC), Centre de Recherches sur les Macromolécules Végétales (CERMAV), Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes (UGA), Université Fédérale Toulouse Midi-Pyrénées, Interactions Microbiennes dans la Rhizosphère et les Racines, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-MetaToul-MetaboHUB, Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC)-Institut de Chimie de Toulouse (ICT-FR 2599), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Institut de Chimie du CNRS (INC)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD), Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, University of California [Santa Barbara] (UCSB), University of California, Université de Toulouse (UT)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS), MetaToul Agromix, Université de Toulouse (UT)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS)-MetaboHUB-MetaToul, MetaboHUB-Génopole Toulouse Midi-Pyrénées [Auzeville] (GENOTOUL), Université de Toulouse (UT)-Université de Toulouse (UT)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-MetaboHUB-Génopole Toulouse Midi-Pyrénées [Auzeville] (GENOTOUL), Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Institut de Chimie de Toulouse (ICT), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Institut Ecologie et Environnement (INEE), Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Fédération de Recherche Fluides, Energie, Réacteurs, Matériaux et Transferts (FERMAT), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Institut National des Sciences Appliquées - Toulouse (INSA Toulouse), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), BIBAC - Chimie analytique et interactions biomolécules - matière molle biomimétique (BIBAC), Institut National des Sciences Appliquées (INSA)-Université de Toulouse (UT)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie de Toulouse (ICT), Université de Toulouse (UT), and ANR-17-EURE-0003,CBH-EUR-GS,CBH-EUR-GS(2017)

Subjects
0301 basic medicine, Hypha, Science, General Physics and Astronomy, Oligosaccharides, Chitin, 02 engineering and technology, Biology, General Biochemistry, Genetics and Molecular Biology, Article, Microbiology, Microbial ecology, 03 medical and health sciences, Fungal biology, Pseudohyphal growth, Symbiosis, Ascomycota, Mycorrhizae, Spore germination, [SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biochemistry [q-bio.BM], Cellular microbiology, Fungal ecology, lcsh:Science, [SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biochemistry [q-bio.BM], [SDV.MP.MYC]Life Sciences [q-bio]/Microbiology and Parasitology/Mycology, Chitosan, Multidisciplinary, Ecology, Phylum, Basidiomycota, Fatty Acids, fungi, Fungi, General Chemistry, Spores, Fungal, 021001 nanoscience & nanotechnology, biology.organism_classification, [SDV.MP.MYC] Life Sciences [q-bio]/Microbiology and Parasitology/Mycology, Spore, 030104 developmental biology, lcsh:Q, 0210 nano-technology, Bacteria, Rhizobium, Signal Transduction
Abstract

Lipo-chitooligosaccharides (LCOs) are signaling molecules produced by rhizobial bacteria that trigger the nodulation process in legumes, and by some fungi that also establish symbiotic relationships with plants, notably the arbuscular and ecto mycorrhizal fungi. Here, we show that many other fungi also produce LCOs. We tested 59 species representing most fungal phyla, and found that 53 species produce LCOs that can be detected by functional assays and/or by mass spectroscopy. LCO treatment affects spore germination, branching of hyphae, pseudohyphal growth, and transcription in non-symbiotic fungi from the Ascomycete and Basidiomycete phyla. Our findings suggest that LCO production is common among fungi, and LCOs may function as signals regulating fungal growth and development., Lipo-chitooligosaccharides (LCOs) are signaling molecules produced by certain bacteria and fungi that establish symbiotic relationships with plants. Here, the authors show that LCOs are produced also by many other, non-symbiotic fungi, and regulate fungal growth and development.

Published
2020

5. Regiocontrolled syntheses of FAHFAs and LC-MS/MS differentiation of regioisomers

Author

Thierry Durand, Julien Faugere, Laurence Balas, Sylvie Caspar-Bauguil, Justine Bertrand-Michel, Corinne Lefort, Fanny Viars, Dominique Langin, Institut des Biomolécules Max Mousseron [Pôle Chimie Balard] (IBMM), Ecole Nationale Supérieure de Chimie de Montpellier (ENSCM)-Institut de Chimie du CNRS (INC)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), MetaToul-MetaboHUB, Génopole Toulouse Midi-Pyrénées [Auzeville] (GENOTOUL), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), and CHU Toulouse [Toulouse]

Subjects
0301 basic medicine, chemistry.chemical_classification, Carboxylic acid, Acetylide, Organic Chemistry, Epoxide, Alkyne, Total synthesis, Biochemistry, 03 medical and health sciences, chemistry.chemical_compound, 030104 developmental biology, chemistry, Structural isomer, [CHIM]Chemical Sciences, Organic chemistry, Physical and Theoretical Chemistry, Boron trifluoride, Carbanion
Abstract

International audience; An efficient regiospecific total synthesis of several branched fatty acyl hydroxyl-fatty acids (FAHFA) has been achieved from available terminal alkenes and alkynes. The key steps feature a boron trifluoride mediated epoxide ring opening with acetylide carbanions, followed by hydrogenation of the alkyne function. The carboxylic acid of the hydroxylated chains is introduced at the last step of the synthesis to allow the esterification of the branched hydroxyl group by fatty acids beforehand. The chemical syntheses of a “linear” FAHFA and a branched FAHFA analog containing a Z-olefin in the hydroxyl-fatty acid chain are also reported. A LC-MS/MS method has been developed. Several reversed phase columns were compared. Regioisomers were separated.

Published
2016

6. Fatty acids from fat cell lipolysis do not activate an inflammatory response but are stored as triacylglycerols in adipose tissue macrophages

Author

Diane Beuzelin, Geneviève Tavernier, Sylvie Caspar-Bauguil, Christiane Pecher, Dominique Langin, Marie Adeline Marques, Alexia Zakaroff-Girard, Marianne Houssier, Corinne Lefort, Isabelle K. Vila, Lucile Mir, Sarah Nicolas, Cedric Moro, Catherine Ines Kolditz, and Etienne Mouisel

Subjects
Male, medicine.medical_specialty, Lipolysis, Endocrinology, Diabetes and Metabolism, Adipose tissue macrophages, Palmitic Acid, Adipose tissue, Adrenergic beta-3 Receptor Agonists, Dioxoles, White adipose tissue, Cell Line, Mice, chemistry.chemical_compound, Insulin resistance, Internal medicine, Adipocyte, Adipocytes, Internal Medicine, medicine, Animals, Humans, adipocyte protein 2, Triglycerides, Inflammation, Mice, Knockout, biology, Chemistry, Macrophages, Stem Cells, Fatty Acids, medicine.disease, Toll-Like Receptor 4, Endocrinology, Adipose Tissue, Lipogenesis, biology.protein
Abstract

Activation of macrophages by fatty acids (FAs) is a potential mechanism linking obesity to adipose tissue (AT) inflammation and insulin resistance. Here, we investigated the effects of FAs released during adipocyte lipolysis on AT macrophages (ATMs).Human THP-1 macrophages were treated with media from human multipotent adipose-derived stem (hMADS) adipocytes stimulated with lipolytic drugs. Macrophages were also treated with mixtures of FAs and an inhibitor of Toll-like receptor 4, since this receptor is activated by saturated FAs. Levels of mRNA and the secretion of inflammation-related molecules were measured in macrophages. FA composition was determined in adipocytes, conditioned media and macrophages. The effect of chronic inhibition or acute activation of fat cell lipolysis on ATM response was investigated in vivo in mice.Whereas palmitic acid alone activates THP-1, conditioned media from hMADS adipocyte lipolysis had no effect on IL, chemokine and cytokine gene expression, and secretion by macrophages. Mixtures of FAs representing de novo lipogenesis or habitual dietary conditions also had no effect. FAs derived from adipocyte lipolysis were taken up by macrophages and stored as triacylglycerol droplets. In vivo, chronic treatment with an antilipolytic drug did not modify gene expression and number of ATMs in mice with intact or defective Tlr4. Stimulation of adipocyte lipolysis increased storage of neutral lipids by macrophages without change in number and phenotype.Our data suggest that adipocyte lipolysis does not activate inflammatory pathways in ATMs, which instead may act as scavengers of FAs.

Published
2015

7. Immune Cell Toll-like Receptor 4 Mediates the Development of Obesity- and Endotoxemia-Associated Adipose Tissue Fibrosis

Author

Jacques Grober, Vladimir Stich, Philippe Gui, Corinne Lefort, Geneviève Tavernier, Virginie Bourlier, Isabelle K. Vila, Lenka Rossmeislová, Lucile Mir, Katie Louche, Anne Bouloumié, Nathalie Viguerie, Pierre Marie Badin, Balbine Roussel, Alexia Zakaroff-Girard, Dominique Langin, Cedric Moro, Marie Adeline Marques, Laurent Monbrun, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Franco-Czech Laboratory for Clinical Research on Obesity, Charles University [Prague] (CU)-Institut National de la Santé et de la Recherche Médicale (INSERM), PHOTONIQUE (XLIM-PHOTONIQUE), XLIM (XLIM), Université de Limoges (UNILIM)-Centre National de la Recherche Scientifique (CNRS)-Université de Limoges (UNILIM)-Centre National de la Recherche Scientifique (CNRS), Sérine protéases et physiopathologie de l'unité neurovasculaire, Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Lipides - Nutrition - Cancer (U866) (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA), Laboratoire d'Excellence : Lipoprotéines et Santé : prévention et Traitement des maladies Inflammatoires et du Cancer (LabEx LipSTIC), Institut National de la Recherche Agronomique (INRA)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université Paris-Sud - Paris 11 (UP11)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut Gustave Roussy (IGR)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Université de Bourgogne (UB)-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER-Institut National de la Santé et de la Recherche Médicale (INSERM)-Fédération Francophone de la Cancérologie Digestive, FFCD-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université de Montpellier (UM), Forschungsinstitut für Rationalisierung e.V. (FIR) an der RWTH Aachen, Franco-czech Laboratory for clinical research on obesity, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), I.K.V. was supported by fellowships from Inserm and Région Midi-Pyrénées. This work was supported by grants from Agence Nationale de la Recherche (LIPOB and OBELIP projects), Région Midi-Pyrénées, Fondation pour la Recherche Médicale, and the Commission of the European Communities (projects DIABAT, HEPADIP, and ADAPT) (to D.L.) and by a grant from Société Francophone du Diabète (to C.M.)., Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Departament Geodinàmica i Geofísica, Facultat de Geologia, Institut National de la Recherche Agronomique (INRA)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université Paris-Sud - Paris 11 (UP11)-École pratique des hautes études (EPHE)-Institut Gustave Roussy (IGR)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Université de Bourgogne (UB)-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)-Centre Régional de Lutte contre le cancer - Centre Georges-François Leclerc (CRLCC - CGFL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Fédération Francophone de la Cancérologie Digestive, FFCD-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Etablissement français du sang [Bourgogne-France-Comté] (EFS [Bourgogne-France-Comté])-Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire [Besançon] (CHRU Besançon)-Université de Franche-Comté (UFC)-Université de Montpellier (UM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Charles University [Prague], Charles University [Prague]-Institut National de la Santé et de la Recherche Médicale (INSERM), Simon, Marie Francoise, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut Gustave Roussy (IGR)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Université de Bourgogne (UB)-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER-Institut National de la Santé et de la Recherche Médicale (INSERM)-Fédération Francophone de la Cancérologie Digestive, FFCD-Université de Montpellier (UM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut des Maladies Métaboliques et Cardiovasculaires ( I2MC ), Université Paul Sabatier - Toulouse 3 ( UPS ) -Hôpital de Rangueil-Institut National de la Santé et de la Recherche Médicale ( INSERM ), PHOTONIQUE ( XLIM-PHOTONIQUE ), XLIM ( XLIM ), Université de Limoges ( UNILIM ) -Centre National de la Recherche Scientifique ( CNRS ) -Université de Limoges ( UNILIM ) -Centre National de la Recherche Scientifique ( CNRS ), Université de Caen Normandie ( UNICAEN ), Normandie Université ( NU ) -Normandie Université ( NU ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Lipides - Nutrition - Cancer (U866) ( LNC ), Université de Bourgogne ( UB ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon ( ENSBANA ), Charles University [Prague]-Institut National de la Santé et de la Recherche Médicale ( INSERM ), U858 Institut de médecine moléculaire de Rangueil (I2MR), and Institut National de la Santé et de la Recherche Médicale

Subjects
Lipopolysaccharides, MESH: Signal Transduction, MESH: Inflammation, MESH : Toll-Like Receptor 4, Adipose tissue, MESH : Adipocytes, MESH : Lipopolysaccharides, Mice, chemistry.chemical_compound, Fibrosis, Adipocyte, Adipocytes, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, MESH: Obesity, MESH: Animals, lcsh:QH301-705.5, Mice, Inbred C3H, Toll-like receptor, MESH : Diet, High-Fat, MESH: Toll-Like Receptor 4, 3. Good health, MESH: Insulin Resistance, Adipose Tissue, MESH: Fibrosis, MESH : Fibrosis, [SDV.IMM]Life Sciences [q-bio]/Immunology, MESH : Obesity, MESH : Insulin Resistance, MESH: Adipose Tissue, Signal Transduction, medicine.medical_specialty, [SDV.IMM] Life Sciences [q-bio]/Immunology, Adipose tissue macrophages, Biology, Diet, High-Fat, MESH : Adipose Tissue, General Biochemistry, Genetics and Molecular Biology, Immune system, MESH : Mice, Inbred C3H, Internal medicine, MESH : Mice, medicine, Animals, Humans, Obesity, MESH: Mice, Inbred C3H, MESH: Mice, MESH: Adipocytes, Inflammation, MESH : Signal Transduction, MESH : Inflammation, MESH: Humans, MESH : Endotoxemia, MESH : Humans, 3T3-L1, medicine.disease, MESH : Disease Models, Animal, Endotoxemia, Toll-Like Receptor 4, Disease Models, Animal, MESH: Diet, High-Fat, Endocrinology, lcsh:Biology (General), chemistry, MESH: Endotoxemia, MESH : Animals, Insulin Resistance, MESH: Disease Models, Animal, MESH: Lipopolysaccharides, Adipocyte hypertrophy
Abstract

International audience; Adipose tissue fibrosis development blocks adipocyte hypertrophy and favors ectopic lipid accumulation. Here, we show that adipose tissue fibrosis is associated with obesity and insulin resistance in humans and mice. Kinetic studies in C3H mice fed a high-fat diet show activation of macrophages and progression of fibrosis along with adipocyte metabolic dysfunction and death. Adipose tissue fibrosis is attenuated by macrophage depletion. Impairment of Toll-like receptor 4 signaling protects mice from obesity-induced fibrosis. The presence of a functional Toll-like receptor 4 on adipose tissue hematopoietic cells is necessary for the initiation of adipose tissue fibrosis. Continuous low-dose infusion of the Toll-like receptor 4 ligand, lipopolysaccharide, promotes adipose tissue fibrosis. Ex vivo, lipopolysaccharide-mediated induction of fibrosis is prevented by antibodies against the profibrotic factor TGFβ1. Together, these results indicate that obesity and endotoxemia favor the development of adipose tissue fibrosis, a condition associated with insulin resistance, through immune cell Toll-like receptor 4.

Published
2014

8. The Transcriptional Coactivator Peroxisome Proliferator–Activated Receptor (PPAR)γ Coactivator-1α and the Nuclear Receptor PPARα Control the Expression of Glycerol Kinase and Metabolism Genes Independently of PPARγ Activation in Human White Adipocytes

Author

Thierry Pineau, Dominique Langin, Claire Tiraby, Nathalie Viguerie, Anne Mazzucotelli, Jean-Sébastien Annicotte, Juan Hidalgo, Geneviève Tavernier, Karine Clément, Aline Mairal, Emmanuelle Lepin, Paul Delmar, Eva Klimcakova, Lluis Fajas, Corinne Lefort, and Sébastien Déjean

Subjects
Regulation of gene expression, chemistry.chemical_classification, 0303 health sciences, Reporter gene, Glycerol kinase, Endocrinology, Diabetes and Metabolism, Peroxisome proliferator-activated receptor, Alpha (ethology), 030209 endocrinology & metabolism, Biology, Cell biology, 03 medical and health sciences, 0302 clinical medicine, chemistry, Biochemistry, Nuclear receptor, Coactivator, Gene expression, Internal Medicine, 030304 developmental biology
Abstract

OBJECTIVE—The purpose of this work was to determine the pattern of genes regulated by peroxisome proliferator–activated receptor (PPAR) γ coactivator 1α (PGC-1α) in human adipocytes and the involvement of PPARα and PPARγ in PGC-1α transcriptional action. RESEARCH DESIGN AND METHODS—Primary cultures of human adipocytes were transduced with a PGC-1α adenovirus and treated with PPARγ and PPARα agonists. Variation in gene expression was assessed using pangenomic microarrays and quantitative RT-PCR. To investigate glycerol kinase (GyK), a target of PGC-1α, we measured enzymatic activity and glycerol incorporation into triglycerides. In vivo studies were performed on wild-type and PPARα−/− mice. The GyK promoter was studied using chromatin immunoprecipitation and promoter reporter gene assays. RESULTS—Among the large number of genes regulated by PGC-1α independently of PPARγ, new targets involved in metabolism included the gene encoding GyK. The induction of GyK by PGC-1α was observed at the levels of mRNA, enzymatic activity, and glycerol incorporation into triglycerides. PPARα was also upregulated by PGC-1α. Its activation led to an increase in GyK expression and activity. PPARα was shown to bind and activate the GyK promoter. Experiments in mice confirmed the role of PGC-1α and PPARα in the regulation of GyK in vivo. CONCLUSIONS—This work uncovers novel pathways regulated by PGC-1α and reveals that PPARα controls gene expression in human white adipocytes. The induction of GyK by PGC-1α and PPARα may promote a futile cycle of triglyceride hydrolysis and fatty acid reesterification.

Published
2007

9. CO-44: Les peptides natriurétiques stimulent le transport de glucose dans l'adipocyte humain : relation avec la sensibilité à l'insuline

Author

Valentin Barquissau, Nathalie Viguerie, Corinne Lefort, Peter Arner, Pauline Morigny, Katie Louche, Cedric Moro, Christian Carpéné, Mikael Rydén, Marine Coué, and Dominique Langin

Subjects
Endocrinology, Endocrinology, Diabetes and Metabolism, Internal Medicine, General Medicine
Abstract

Introduction Bien qu'une association robuste entre une diminution des niveaux circulants de peptides natriuretiques (PN) et un risque accru de diabete de type 2 a ete rapportee chez l'homme, il n'y a, a ce jour, aucune evidence directe d'une effet des PN sur la sensibilite a l'insuline globale ou dans un tissu cible. Materiels et Methodes L'expression genique des recepteurs aux PN a ete mesuree par RT-qPCR dans des biopsies de tissu adipeux sous-cutane de deux cohortes europeennes independantes. Le transport de glucose a ete mesure sur des adipocytes humains isoles et sur des adipocytes hMADS ( human multipotent adipose-derived stem cell ) en culture. Les experiences de flux metaboliques et de signalisation ont ete effectuees sur hMADS en culture. Resultats Nous demontrons ici que l'expression du recepteur biologiquement actif aux PN de type A (NPRA) diminue tandis que celle du recepteur de clairance de type C (NPRC) augmente avec le degre d'obesite. L'expression du NPRA correle negativement avec la glycemie a jeun et est diminue chez des individus pre-diabetiques et diabetiques de type 2. L'expression du NPRA correle aussi negativement avec l'insulino-resistance (r=− 0,65, p Conclusions Collectivement, nos donnees supportent un role des PN dans la regulation du metabolisme du glucose et de la sensibilite a l'insuline en stimulant le transport de glucose dans l'adipocyte humain. La signalisation aux PN pourrait constituer une cible potentielle pour ameliorer l'insulinoresistance associee a l'obesite.

Published
2016

10. Acquirement of Brown Fat Cell Features by Human White Adipocytes

Author

Frédéric Bouillaud, Daniel Ricquier, Corinne Lefort, Dominique Langin, Geneviève Tavernier, Dominique Larrouy, and Claire Tiraby

Subjects
Male, Time Factors, Transcription, Genetic, Palmitic Acid, Respiratory chain, Receptors, Cytoplasmic and Nuclear, Adipose tissue, White adipose tissue, Biochemistry, Ion Channels, Mice, Adipose Tissue, Brown, Brown adipose tissue, Adipocytes, Promoter Regions, Genetic, Beta oxidation, Uncoupling Protein 1, Reverse Transcriptase Polymerase Chain Reaction, Flow Cytometry, Recombinant Proteins, Thermogenin, Mitochondria, medicine.anatomical_structure, Rosiglitazone, medicine.drug, Chloramphenicol O-Acetyltransferase, Transcriptional Activation, medicine.medical_specialty, DNA, Complementary, Blotting, Western, Green Fluorescent Proteins, Cytochrome c Group, Biology, Models, Biological, Adenoviridae, Mitochondrial Proteins, Internal medicine, Coactivator, medicine, Animals, Humans, Obesity, RNA, Messenger, Molecular Biology, Membrane Proteins, Cell Biology, Rats, Oxygen, Luminescent Proteins, Endocrinology, Carrier Proteins, Transcription Factors
Abstract

Obesity, i.e. an excess of white adipose tissue (WAT), predisposes to the development of type 2 diabetes and cardiovascular disease. Brown adipose tissue is present in rodents but not in adult humans. It expresses uncoupling protein 1 (UCP1) that allows dissipation of energy as heat. Peroxisome proliferator-activated receptor gamma (PPAR gamma) and PPAR gamma coactivator 1 alpha (PGC-1 alpha) activate mouse UCP1 gene transcription. We show here that human PGC-1 alpha induced the activation of the human UCP1 promoter by PPAR gamma. Adenovirus-mediated expression of human PGC-1 alpha increased the expression of UCP1, respiratory chain proteins, and fatty acid oxidation enzymes in human subcutaneous white adipocytes. Changes in the expression of other genes were also consistent with brown adipocyte mRNA expression profile. PGC-1 alpha increased the palmitate oxidation rate by fat cells. Human white adipocytes can therefore acquire typical features of brown fat cells. The PPAR gamma agonist rosiglitazone potentiated the effect of PGC-1 alpha on UCP1 expression and fatty acid oxidation. Hence, PGC-1 alpha is able to direct human WAT PPAR gamma toward a transcriptional program linked to energy dissipation. However, the response of typical white adipocyte targets to rosiglitazone treatment was not altered by PGC-1 alpha. UCP1 mRNA induction was shown in vivo by injection of the PGC-1 alpha adenovirus in mouse white fat. Alteration of energy balance through an increased utilization of fat in WAT may be a conceivable strategy for the treatment of obesity.

Published
2003

11. Chronic TNFalpha and cAMP pre-treatment of human adipocytes alter HSL, ATGL and perilipin to regulate basal and stimulated lipolysis

Author

Aline Mairal, Véronic Bezaire, Corinne Lefort, Dominique Langin, Rodica Anesia, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de Biochimie [Purpan], Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut Fédératif de Biologie (IFB) - Hôpital Purpan, Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse]-Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse], Simon, Marie Francoise, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de Biochimie [CHU Toulouse], Institut Fédératif de Biologie (IFB), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Pôle Biologie [CHU Toulouse], and Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)

Subjects
medicine.medical_specialty, Hormone-sensitive lipase, Perilipin-1, Lipolysis, Biophysics, Biology, Biochemistry, Adipose triglyceride lipase, 03 medical and health sciences, 0302 clinical medicine, Protein kinase A, Structural Biology, Internal medicine, Lipid droplet, Genetics, medicine, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, TNFα, Adipocytes, Cyclic AMP, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Phosphorylation, Molecular Biology, 030304 developmental biology, 0303 health sciences, Tumor Necrosis Factor-alpha, Colforsin, Cell Biology, Lipase, Sterol Esterase, Phosphoproteins, Endocrinology, 030220 oncology & carcinogenesis, Perilipin, Carrier Proteins, Forskolin
Abstract

International audience; We examined the effects of chronic TNFalpha and dibutyryl-cAMP (Db-cAMP) pre-treatment on the lipolytic machinery of human hMADS adipocytes. TNFalpha decreased adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) protein content and triglycerides (TG)-hydrolase activity but increased basal lipolysis due to a marked reduction in perilipin (PLIN) protein content. Conversely, Db-cAMP increased ATGL and HSL protein content but prevented PLIN phosphorylation, the net result being accentuated basal lipolysis. In forskolin-stimulated conditions, TNFalpha and Db-cAMP pre-treatment decreased stimulated TG-hydrolase activity and impaired PLIN phosphorylation. Together, this resulted in a severely attenuated response to forskolin-stimulated lipolysis.

Published
2009

12. Contribution of Adipose Triglyceride Lipase and Hormone-sensitive Lipase to Lipolysis in hMADS Adipocytes

Author

Peter Arner, Anne-Marie Rodriguez, Rodica Anesia, Jurga Laurencikiene, Amandine Girousse, Dominique Langin, Johan W. E. Jocken, Véronic Bezaire, Gérard Ailhaud, Christian Dani, Aline Mairal, Britta M Stenson, Corinne Lefort, Mikael Rydén, Carole Ribet, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of medicine [Stockholm], Karolinska Institutet [Stockholm]-Karolinska University Hospital [Stockholm], Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Institut de Signalisation, Biologie du Développement et Cancer, Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA), Laboratoire de Biochimie [Purpan], Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut Fédératif de Biologie (IFB) - Hôpital Purpan, Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse]-Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse], Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Nice Sophia Antipolis (1965 - 2019) (UNS), Laboratoire de Biochimie [CHU Toulouse], Institut Fédératif de Biologie (IFB), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Pôle Biologie [CHU Toulouse], Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Simon, Marie Francoise, Humane Biologie, RS: NUTRIM - R1 - Metabolic Syndrome, and CHU Toulouse [Toulouse]-Institut Fédératif de Biologie (IFB) - Hôpital Purpan

Subjects
medicine.medical_specialty, Lipolysis, Green Fluorescent Proteins, 030209 endocrinology & metabolism, Hormone-sensitive lipase, Biochemistry, 03 medical and health sciences, chemistry.chemical_compound, Cytosol, 0302 clinical medicine, Internal medicine, Lipid droplet, Adipocytes, medicine, Humans, RNA, Small Interfering, Lipase, Molecular Biology, Cells, Cultured, 030304 developmental biology, chemistry.chemical_classification, 0303 health sciences, Esterification, biology, Fatty acid metabolism, Catabolism, Hydrolysis, Colforsin, Fatty Acids, Fatty acid, Cell Biology, 1-Acylglycerol-3-Phosphate O-Acyltransferase, Sterol Esterase, Metabolism and Bioenergetics, Endocrinology, chemistry, Adipose triglyceride lipase, biology.protein, Energy Metabolism
Abstract

International audience; Lipolysis is the catabolic pathway by which triglycerides are hydrolyzed into fatty acids. Adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) have the capacity to hydrolyze in vitro the first ester bond of triglycerides, but their respective contributions to whole cell lipolysis in human adipocytes is unclear. Here, we have investigated the roles of HSL, ATGL, and its coactivator CGI-58 in basal and forskolin-stimulated lipolysis in a human white adipocyte model, the hMADS cells. The hMADS adipocytes express the various components of fatty acid metabolism and show lipolytic capacity similar to primary cultured adipocytes. We show that lipolysis and fatty acid esterification are tightly coupled except in conditions of stimulated lipolysis. Immunocytochemistry experiments revealed that acute forskolin treatment promotes HSL translocation from the cytosol to small lipid droplets and redistribution of ATGL from the cytosol and large lipid droplets to small lipid droplets, resulting in enriched colocalization of the two lipases. HSL or ATGL overexpression resulted in increased triglyceride-specific hydrolase capacity, but only ATGL overexpression increased whole cell lipolysis. HSL silencing had no effect on basal lipolysis and only partially reduced forskolin-stimulated lipolysis. Conversely, silencing of ATGL or CGI-58 significantly reduced basal lipolysis and essentially abolished forskolin-stimulated lipolysis. Altogether, these results suggest that ATGL/CGI-58 acts independently of HSL and precedes its action in the sequential hydrolysis of triglycerides in human hMADS adipocytes.

Published
2009

13. Adipogenesis-related increase of semicarbazide-sensitive amine oxidase and monoamine oxidase in human adipocytes

Author

Sandy Bour, Philippe Valet, Christian Carpéné, Sandra Grès, Jean-Sébastien Saulnier-Blache, Antonio Zorzano, Martin Wabitsch, Danièle Daviaud, Corinne Lefort, D. Prévot, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Departamento de Bioquimica y Biologia Molecular, Universidad de Barcelona, Department of Pediatrics and Adolescent Medicine, Universität Ulm - Ulm University [Ulm, Allemagne], Simon, Marie Francoise, and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
AOC3, MESH: 3T3 Cells, Adipose tissue, Biochemistry, Mice, chemistry.chemical_compound, 0302 clinical medicine, Adipocyte, Adipocytes, MESH: Animals, 0303 health sciences, Adipogenesis, MESH: Middle Aged, Cell Differentiation, 3T3 Cells, General Medicine, Middle Aged, MESH: Infant, medicine.anatomical_structure, Female, Amine Oxidase (Copper-Containing), Adult, MESH: Cell Differentiation, medicine.medical_specialty, Amine oxidase, Monoamine oxidase, Biology, MESH: Monoamine Oxidase, 3T3 cells, 03 medical and health sciences, 3T3-L1 Cells, Internal medicine, medicine, Animals, Humans, Cell Lineage, RNA, Messenger, Monoamine Oxidase, MESH: Mice, MESH: Adipocytes, 030304 developmental biology, MESH: RNA, Messenger, MESH: Humans, Infant, MESH: Adult, MESH: Cell Lineage, MESH: 3T3-L1 Cells, Endocrinology, chemistry, MESH: Amine Oxidase (Copper-Containing), MESH: Adipogenesis, MESH: Female, 030217 neurology & neurosurgery, Ex vivo
Abstract

International audience; A strong induction of semicarbazide-sensitive amine oxidase (SSAO) has previously been reported during murine preadipocyte lineage differentiation but it remains unknown whether this emergence also occurs during adipogenesis in man. Our aim was to compare SSAO and monoamine oxidase (MAO) expression during in vitro differentiation of human preadipocytes and in adipose and stroma-vascular fractions of human fat depots. A human preadipocyte cell strain from a patient with Simpson-Golabi-Behmel syndrome was first used to follow amine oxidase expression during in vitro differentiation. Then, human preadipocytes isolated from subcutaneous adipose tissues were cultured under conditions promoting ex vivo adipose differentiation and tested for MAO and SSAO expression. Lastly, human adipose tissue was separated into mature adipocyte and stroma-vascular fractions for analyses of MAO and SSAO at mRNA, protein and activity levels. Both SSAO and MAO were increased from undifferentiated preadipocytes to lipid-laden cells in all the models: 3T3-F442A and 3T3-L1 murine lineages, human SGBS cell strain or human preadipocytes in primary culture. In human subcutaneous adipose tissue, the adipocyte-enriched fraction exhibited seven-fold higher amine oxidase activity and contained three- to seven-fold higher levels of mRNAs encoded by MAO-A, MAO-B, AOC3 and AOC2 genes than the stroma-vascular fraction. MAO-A and AOC3 genes accounted for the majority of their respective MAO and SSAO activities in human adipose tissue. Most of the SSAO and MAO found in adipose tissue originated from mature adipocytes. Although the mechanism and role of adipogenesis-related increase in amine oxidase expression remain to be established, the resulting elevated levels of amine oxidase activities found in human adipocytes may be of potential interest for therapeutic intervention in obesity.

Published
2007

14. The suppression of osmoinduced proline response of Brassica napus L. var oleifera leaf discs by polyunsaturated fatty acids and methyl-jasmonate

Author

François Larher, Corinne Lefort, Valérie Maerskalck, Neil R. J. Emery, Ronan Sulpice, Valérie Huguet-Robert, Interactions Cellulaires et Moléculaires, Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-IFR98-Centre National de la Recherche Scientifique (CNRS), and Université de Rennes (UR)-IFR98-Centre National de la Recherche Scientifique (CNRS)

Subjects
0106 biological sciences, Osmotic shock, Proline, Linoleic acid, Water stress, Plant Science, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], 01 natural sciences, 03 medical and health sciences, chemistry.chemical_compound, Lipoxygenase, Genetics, [SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biochemistry [q-bio.BM], Fatty acids, Abscisic acid, Methyl-jasmonate, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, chemistry.chemical_classification, 0303 health sciences, Methyl jasmonate, biology, Brassica napus, food and beverages, [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology, General Medicine, Oxylipin, [SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biomolecules [q-bio.BM], chemistry, Biochemistry, biology.protein, lipids (amino acids, peptides, and proteins), Agronomy and Crop Science, 010606 plant biology & botany, Polyunsaturated fatty acid
Abstract

When subjected in vitro to upshock osmotic stress, canola leaf discs accumulate large amounts of proline. In this study, we investigated the regulatory effect exerted on the osmoinduced proline response by polyunsaturated fatty acids (PUFAs) and derivatives of the oxylipin pathway. When supplied to the stressing medium, PUFAs were found to inhibit proline accumulation, with α and γ-linolenic acid (C18:3) being more effective than linoleic acid (C18:2). The amount of accumulated proline increased to 200 μmol g −1 dry weight (DW) and remained constant in leaf discs subjected for 8 h to a stress medium containing 350 g l −1 PEG 6000 added with PUFAs, compared with levels observed in control discs treated with PEG that continued to increase to approximately 600 μmol g −1 DW regularly for up to 24 h. The suppressing effect of PUFAs was mimicked by methyl-jasmonate (Me-JA). Whatever the mediator used, this effect was dependent on its concentration and on the moment when osmotic stress was applied: γ-C18:3>α-C18:3>C18:2. An identical effect was observed with 12-oxo-phytodienoic acid (12-OPDA). In addition, the suppressing effect of Me-JA was found to counteract the promoting effect of abscisic acid (ABA). Collectively, these results demonstrated that proline accumulation by canola leaf explants subjected in vitro to osmotic stress could be partly suppressed by exogenously supplied free fatty acids (FAs) and by products resulting from their hydroperoxidation by lipoxygenase (LOXs). The physiological relevance of these findings is discussed.

Published
2003

15. Hypocaloric diet reduces exercise-induced alpha 2-adrenergic antilipolytic effect and alpha 2-adrenergic receptor mRNA levels in adipose tissue of obese women

Author

Max Lafontan, Michel Berlan, Nathalie Viguerie, F. Marion-Latard, J. Hejnova, Hana Suljkovicova, Corinne Lefort, Vladimir Stich, and Dominique Langin

Subjects
Adult, Glycerol, medicine.medical_specialty, Microdialysis, Sympathetic nervous system, Adrenergic receptor, Diet, Reducing, Endocrinology, Diabetes and Metabolism, Clinical Biochemistry, Adipose tissue, Stimulation, Physical exercise, Fatty Acids, Nonesterified, Biochemistry, Endocrinology, Phentolamine, Receptors, Adrenergic, alpha-2, Internal medicine, Abdomen, Receptors, Adrenergic, beta, medicine, Humans, Lactic Acid, Obesity, RNA, Messenger, Exercise, Chemistry, Biochemistry (medical), Osmolar Concentration, medicine.anatomical_structure, Adipose Tissue, Regional Blood Flow, Catecholamine, Female, Energy Intake, Extracellular Space, medicine.drug
Abstract

Previous investigations have shown that alpha 2-adrenoceptor (alpha 2-AR) stimulation blunts lipid mobilization during physiological activation of the sympathetic nervous system promoted by exercise in sc abdominal adipose tissue (SCAAT) in obese men. To investigate the effect of a low calorie diet (LCD) on the alpha 2-adrenergic responsiveness and on the expression of alpha 2-AR and beta 2-adrenoceptor (beta 2-AR) in SCAAT, 11 obese women (weight: 99.1 +/- 4.6 kg; body mass index: 34.3 +/- 1.1 kg/m(2)) received a 12-wk diet providing 500 kcal/d less than their usual diet. The exercise-induced alpha 2-adrenergic antilipolytic effect was investigated in SCAAT before and at the end of LCD. Changes in extracellular glycerol concentration and local blood flow were measured in SCAAT during a 45-min exercise bout (50% of heart rate reserve) using a control microdialysis probe and a probe supplemented with the alpha2-AR antagonist phentolamine. SCAAT biopsies were performed for determination of mRNA levels using RT-competitive PCR. Plasma catecholamine responses to exercise bout were not different before and at the end of LCD. Before LCD, the exercise-induced increase in extracellular glycerol concentration was potentiated by phentolamine supplementation, while this potentiating effect of the alpha-antagonist was not observed at the end of LCD. No changes were observed for beta 2-AR and hormone-sensitive lipase mRNA levels, while alpha 2-AR mRNA level was significantly decreased in adipose tissue during LCD. These findings show that alpha 2-AR-mediated antilipolytic action is reduced by a moderate hypocaloric diet and that down-regulation of alpha 2-AR mRNA levels may participate in the decrease of the alpha 2-adrenergic effect revealed by microdialysis.

Published
2002

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