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1. 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

2. 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

3. 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

4. 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

5. 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

6. 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

7. 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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