Dominique Langin

Paul Sabatier University - Toulouse III, Tolosa de Llenguadoc, Midi-Pyrénées, France

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Publications (275)1519.66 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Accumulation of visceral adipose tissue correlates with elevated inflammation and increased risk of metabolic diseases. However, little is known about the molecular mechanisms that control its pathological expansion. Transcription factor interferon regulatory factor 5 (IRF5) has been implicated in polarizing macrophages towards an inflammatory phenotype. Here we demonstrate that mice lacking Irf5, when placed on a high-fat diet, show no difference in the growth of their epididymal white adipose tissue (epiWAT) but they show expansion of their subcutaneous white adipose tissue, as compared to wild-type (WT) mice on the same diet. EpiWAT from Irf5-deficient mice is marked by accumulation of alternatively activated macrophages, higher collagen deposition that restricts adipocyte size, and enhanced insulin sensitivity compared to epiWAT from WT mice. In obese individuals, IRF5 expression is negatively associated with insulin sensitivity and collagen deposition in visceral adipose tissue. Genome-wide analysis of gene expression in adipose tissue macrophages highlights the transforming growth factor β1 (TGFB1) gene itself as a direct target of IRF5-mediated inhibition. This study uncovers a new function for IRF5 in controlling the relative mass of different adipose tissue depots and thus insulin sensitivity in obesity, and it suggests that inhibition of IRF5 may promote a healthy metabolic state during this condition.
    Nature medicine 05/2015; DOI:10.1038/nm.3829 · 28.05 Impact Factor
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    ABSTRACT: and Objective: A decrease in skeletal muscle lipolysis and hormone sensitive-lipase (HSL) expression has been linked to insulin resistance in obesity. The purpose of this study was to identify potential intrinsic defects in lipid turnover and lipolysis in myotubes established from obese and type 2 diabetic subjects. Lipid trafficking and lipolysis were measured by pulse-chase assay with radiolabeled substrates in myotubes from non-obese/non-diabetic (lean), obese/non-diabetic (obese) and obese/diabetic (T2D) subjects. Lipolytic protein content and level of Akt phosphorylation were measured by Western blot. HSL was overexpressed by adenovirus-mediated gene delivery. Myotubes established from obese and T2D subjects had lower lipolysis (-30-40%) when compared to lean, using oleic acid as labelled precursor. Incorporation of oleic acid into diacylglycerol (DAG) and free fatty acid (FFA) level was lower in T2D myotubes, and acetate incorporation into FFA and complex lipids was also lower in obese and T2D subjects. Both protein expression of HSL (but not ATGL) and changes in DAG during lipolysis were markedly lower in cells from obese and T2D when compared to lean subjects. Insulin-stimulated glycogen synthesis (-60%) and Akt phosphorylation (-90%) were lower in myotubes from T2D, however, overexpression of HSL in T2D myotubes did not rescue the diabetic phenotype. Intrinsic defects in lipolysis and HSL expression co-exist with reduced insulin action in myotubes from obese T2D subjects. Despite reductions in intramyocellular lipolysis and HSL expression, overexpression of HSL did not rescue defects in insulin action in skeletal myotubes from obese T2D subjects. Copyright © 2015. Published by Elsevier B.V.
    Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 03/2015; DOI:10.1016/j.bbalip.2015.03.005 · 4.50 Impact Factor
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    ABSTRACT: Adipocytes are cells specialized for storage of neutral lipids. This storage capacity is dependent on lipogenesis and is diminished in obesity. The reason for the decline in lipogenic activity of adipocytes in obesity remains unknown. Recent data show that lipogenesis in liver is regulated by pathways initiated by endoplasmic reticulum stress (ERS). Thus, we aimed at investigating the effect of ERS on lipogenesis in adipose cells. Preadipocytes were isolated from subcutaneous abdominal adipose tissue from obese volunteers and in vitro differentiated into adipocytes. ERS was induced pharmacologically by thapsigargin (TG) or tunicamycin (TM). Activation of Unfolded Protein Response pathway (UPR) was monitored on the level of eIF2a phosphorylation and mRNA expression of downstream targets of UPR sensors. Adipogenic and lipogenic capacity was evaluated by Oil Red O staining, measurement of incorporation of radio-labelled glucose or acetic acid into lipids and mRNA analysis of adipogenic/lipogenic markers. Exposition of adipocytes to high doses of TG (100 nM) and TM (1 μg/ml) for 1-24 hours enhanced expression of several UPR markers (HSPA5, EDEM1, ATF4, XBP1s) and phosphorylation of eIF2α. This acute ERS substantially inhibited expression of lipogenic genes (DGAT2, FAS, SCD1) and glucose incorporation into lipids. Moreover, chronic exposure of preadipocytes to low dose of TG (2.5 nM) during the early phases of adipogenic conversion of preadipocytes impaired both, lipogenesis and adipogenesis. On the other hand, chronic low ERS had no apparent effect on lipogenesis in mature adipocytes. Acute ERS weakened a capacity of mature adipocytes to store lipids and chronic ERS diminished adipogenic potential of preadipocytes. Copyright © 2015 Elsevier Inc. All rights reserved.
    Biochemical and Biophysical Research Communications 03/2015; 460(3). DOI:10.1016/j.bbrc.2015.03.090 · 2.28 Impact Factor
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    ABSTRACT: Nutrigenomics investigates relationships between nutrients and all genome-encoded molecular entities. This holistic approach requires systems biology to scrutinize the effects of diet on tissue biology. To decipher the adipose tissue (AT) response to diet induced weight changes we focused on key molecular (lipids and transcripts) AT species during a longitudinal dietary intervention. To obtain a systems model, a network approach was used to combine all sets of variables (bio-clinical, fatty acids and mRNA levels) and get an overview of their interactions. AT fatty acids and mRNA levels were quantified in 135 obese women at baseline, after an 8-week low calorie diet (LCD) and after 6 months of ad libitum weight maintenance diet (WMD). After LCD, individuals were stratified a posteriori according to weight change during WMD. A 3 steps approach was used to infer a global model involving the 3 sets of variables. It consisted in inferring intra-omic networks with sparse partial correlations and inter-omic networks with regularized canonical correlation analysis and finally combining the obtained omic-specific network in a single global model. The resulting networks were analyzed using node clustering, systematic important node extraction and cluster comparisons. Overall, AT showed both constant and phase-specific biological signatures in response to dietary intervention. AT from women regaining weight displayed growth factors, angiogenesis and proliferation signaling signatures, suggesting unfavorable tissue hyperplasia. By contrast, after LCD a strong positive relationship between AT myristoleic acid (a fatty acid with low AT level) content and de novo lipogenesis mRNAs was found. This relationship was also observed, after WMD, in the group of women that continued to lose weight. This original system biology approach provides novel insight in the AT response to weight control by highlighting the central role of myristoleic acid that may account for the beneficial effects of weight loss.
    PLoS Computational Biology 01/2015; 11(1):e1004047. DOI:10.1371/journal.pcbi.1004047 · 4.83 Impact Factor
  • Nutrition Clinique et Métabolisme 12/2014; 28. DOI:10.1016/S0985-0562(14)70604-1 · 0.62 Impact Factor
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    ABSTRACT: α-Lipoic acid (α-Lip) is a natural occurring antioxidant with beneficial anti-obesity properties. The aim of this study was to investigate the putative effects of α-Lip on mitochondrial biogenesis and the acquirement of brown-like characteristics by subcutaneous adipocytes from overweight/obese subjects. Thus, fully differentiated human subcutaneous adipocytes were treated with α-Lip (100 and 250μM) for 24h for studies on mitochondrial content and morphology, mitochondrial DNA (mtDNA) copy number, fatty acid oxidation enzymes and brown/beige characteristic genes. The involvement of the Sirtuin1/peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (SIRT1/PGC-1α) pathway was also evaluated. Our results showed that α-Lip increased mitochondrial content in cultured human adipocytes as revealed by electron microscopy and by mitotracker green labeling. Moreover, an enhancement in mtDNA content was observed. This increase was accompanied by an up-regulation of SIRT1 protein levels, a decrease in PGC-1α acetylation and up-regulation of Nuclear respiratory factor 1 (Nrf1) and mitochondrial transcription factor (Tfam) transcription factors. Enhanced oxygen consumption and fatty acid oxidation enzymes, Carnitine palmitoyl transferase 1 and acyl-coenzyme A oxidase (CPT-1 and ACOX) were also observed. Mitochondria from α-Lip-treated adipocytes exhibited some morphological characteristics of brown mitochondria, and α-Lip also induced up-regulation of some brown/beige adipocytes markers such ascell death-inducing DFFA-like effector a (Cidea) and T box 1(Tbx1). Moreover, α-Lip up-regulated PR domain containing 16 (Prdm16) mRNA levels in treated adipocytes. Therefore, our study suggests the ability of α-Lip to promote mitochondrial biogenesis and brown-like remodeling in cultured white subcutaneous adipocytes from overweight/obese donors. Copyright © 2014. Published by Elsevier B.V.
    Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 12/2014; 1851(3). DOI:10.1016/j.bbalip.2014.12.013 · 4.50 Impact Factor
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    ABSTRACT: Brite adipocytes are inducible energy-dissipating cells expressing UCP1 which appear within white adipose tissue of healthy adult individuals. Recruitment of these cells represents a potential strategy to fight obesity and associated diseases. Using human Multipotent Adipose-Derived Stem cells, able to convert into brite adipocytes, we show that arachidonic acid strongly inhibits brite adipocyte formation via a cyclooxygenase pathway leading to secretion of PGE2 and PGF2α. Both prostaglandins induce an oscillatory Ca++ signaling coupled to ERK pathway and trigger a decrease in UCP1 expression and in oxygen consumption without altering mitochondriogenesis. In mice fed a standard diet supplemented with ω6 arachidonic acid, PGF2α and PGE2 amounts are increased in subcutaneous white adipose tissue and associated with a decrease in the recruitment of brite adipocytes. Our results suggest that dietary excess of ω6 polyunsaturated fatty acids present in Western diets, may also favor obesity by preventing the “browning” process to take place.
    12/2014; DOI:10.1016/j.molmet.2014.09.003
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    ABSTRACT: Objectiveα-Lipoic acid (α-LA) is a natural occurring antioxidant with beneficial effects on obesity. The aim of this study was to investigate the putative effects of α-LA on triglyceride accumulation and lipogenesis in subcutaneous adipocytes from overweight/obese subjects and to determine the potential mechanisms involved.Design and Methods Fully differentiated human subcutaneous adipocytes were treated with α-LA (100 and 250 µM) during 24 h for studying triglyceride content, de novo lipogenesis, and levels of key lipogenic enzymes. The involvement of AMP-activated protein kinase (AMPK) activation was also evaluated.Resultsα-LA down-regulated triglyceride content by inhibiting fatty acid esterification and de novo lipogenesis. These effects were mediated by reduction in fatty acid synthase (FAS), stearoyl-coenzyme A desaturase 1, and diacylglycerol O-acyltransferase 1 protein levels. Interestingly, α-LA increased AMPK and acetyl CoA carboxylase phosphorylation, while the presence of the AMPK inhibitor Compound C reversed the inhibition observed on FAS protein levels.Conclusionsα-LA down-regulates key lipogenic enzymes, inhibiting lipogenesis and reducing triglyceride accumulation through the activation of AMPK signaling pathway in human subcutaneous adipocytes from overweight/obese subjects.
    Obesity 10/2014; 22(10). DOI:10.1002/oby.20846 · 4.39 Impact Factor
  • Rudolf Zechner, Dominique Langin
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    ABSTRACT: The breakdown of cellular fat stores fuels energy production and multiple anabolic processes. Albert et al. (2014) demonstrate that the lack of hormone-sensitive lipase, a member of the enzyme trio that catabolizes fat, has pronounced effects on lipid metabolism, glucose homeostasis, and cell signaling in humans.
    Cell Metabolism 08/2014; 20(2):199–201. DOI:10.1016/j.cmet.2014.07.018 · 16.75 Impact Factor
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    ABSTRACT: Weight loss reduces risk factors associated with obesity. However, long-term metabolic improvement remains a challenge. We investigated quantitative gene expression of subcutaneous adipose tissue in obese individuals and its relationship with low calorie diet and long term weight maintenance induced changes in insulin resistance.
    PLoS ONE 07/2014; 9(7):e98707. DOI:10.1371/journal.pone.0098707 · 3.53 Impact Factor
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    ABSTRACT: Objectives: To investigate if inulin-type fructan (ITF) prebiotics could counteract the thiazolidinedione (TZD, PPARγ activator) induced-fat mass gain, without affecting its beneficial effect on glucose homeostasis, in high-fat (HF) diet fed mice. Design and Methods: Male C57bl6/J mice were fed a HF diet alone or supplemented with ITF prebiotics (0.2g/day*mouse) or TZD (30mg pioglitazone/kg body weight*day) or both during 4 weeks. An insulin tolerance test was performed after 3 weeks of treatment. Results: As expected, pioglitazone improved glucose homeostasis and increased adiponectinaemia. Furthermore, it induced an over-expression of several PPARγ target genes in white adipose tissues. ITF prebiotics modulated the pioglitazone-induced PPARγ activation in a tissue-dependent manner. The co-treatment with ITF prebiotics and pioglitazone maintained the beneficial impact of TZD on glucose homeostasis and adiponectinaemia. Moreover, the combination of both treatments reduced fat mass accumulation, circulating lipids and hepatic triglyceride content, suggesting an overall improvement of metabolism. Finally, the co-treatment favored induction of white-to-brown fat conversion in subcutaneous adipose tissue (SAT), thereby leading to the development of brite adipocytes that could increase the oxidative capacity of the tissue. Conclusions: ITF prebiotics decrease adiposity and improve the metabolic response in HF fed mice treated with TZD.
    Obesity 07/2014; 22(7). DOI:10.1002/oby.20733 · 4.39 Impact Factor
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    ABSTRACT: j.celrep.2014.03.062 This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/). SUMMARY Adipose tissue fibrosis development blocks adipo-cyte hypertrophy and favors ectopic lipid accumula-tion. Here, we show that adipose tissue fibrosis is associated with obesity and insulin resistance in hu-mans and mice. Kinetic studies in C3H mice fed a high-fat diet show activation of macrophages and progression of fibrosis along with adipocyte meta-bolic 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 func-tional Toll-like receptor 4 on adipose tissue hemato-poietic cells is necessary for the initiation of adipose tissue fibrosis. Continuous low-dose infusion of the Toll-like receptor 4 ligand, lipopolysaccharide, pro-motes adipose tissue fibrosis. Ex vivo, lipopolysac-charide-mediated induction of fibrosis is prevented by antibodies against the profibrotic factor TGFb1. Together, these results indicate that obesity and en-dotoxemia favor the development of adipose tissue fibrosis, a condition associated with insulin resis-tance, through immune cell Toll-like receptor 4. INTRODUCTION
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    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.
    Cell Reports 04/2014; 7(4). DOI:10.1016/j.celrep.2014.03.062 · 7.21 Impact Factor
  • Peter Arner, Dominique Langin
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    ABSTRACT: Triglycerides in adipose tissue are rapidly mobilized during times of energy needs via lipolysis, a catabolic process that plays important role in whole body triglyceride turnover. Lipolysis is regulated through cell surface receptors via neurotransmitters, hormones, and paracrine factors that activate various intracellular pathways. These pathways converge on the lipid droplet, the site of action of lipases and cofactors. Fat cell lipolysis is also involved in the pathogenesis of metabolic disorders, and recent human studies have underscored its role in disease states such as cancer cachexia and obesity-induced insulin resistance. We highlight here topics and findings with physiological and clinical relevance, namely lipid turnover in human fat cells and the role of lipolysis in cancer cachexia and obesity-induced insulin resistance.
    Trends in Endocrinology and Metabolism 04/2014; DOI:10.1016/j.tem.2014.03.002 · 8.87 Impact Factor
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    ABSTRACT: Introduction Les triglycérides intramusculaires constituent une source d’énergie importante pour le muscle squelettique notamment au cours d’un exercice physique. Des travaux récents suggèrent que l’ATGL (adipose triglyceride lipase) joue un rôle clé dans ce processus. Cependant, peu de données sont actuellement disponibles sur le contrôle de son activité. L’objectif de ce travail était d’étudier le rôle de la protéine G0/G1 Switch Gene 2 (G0S2), récemment décrite comme inhibitrice de l’ATGL dans le tissu adipeux, dans la régulation de la lipolyse et du métabolisme oxydatif musculaire. Matériels et méthodes L’expression de G0S2 a été diminuée, à l’aide de lentivirus contenant des shRNA, dans des cultures primaires de cellules musculaires squelettiques humaines (i.e. myotubes) issues de biopsies de rectus abdominis obtenues chez des volontaires sains. L’activité de l’ATGL, le contenu en triglycérides, la mobilisation et l’oxydation des acides gras, l’oxydation du glucose et la synthèse de glycogène ont été évalués à l’aide de substrats radiomarqués. Les approches métaboliques ont été complétées par des études d’immunofluorescence des mitochondries et d’expression de gènes clés par RT-qPCR. Résultats Nos résultats montrent que G0S2 est exprimé dans les myotubes et qu’il inhibe l’activité de l’ATGL. Son invalidation induit une diminution du pool de triglycérides et une augmentation de la mobilisation et de l’oxydation des acides gras. L’oxydation du glucose et la synthèse de glycogène sont diminuées. L’augmentation du flux d’acides gras s’accompagne d’une hausse de la masse et du potentiel de membrane des mitochondries. Ces effets seraient potentiellement médiés par l’induction de gènes cibles du Peroxysome Proliferator Activated Receptor δ (PPARδ). Conclusion Ces résultats indiquent que G0S2 joue un rôle majeur dans la régulation de la lipolyse et du métabolisme oxydatif musculaire, en modulant le flux d’acides gras et l’expression de gènes cibles de PPARδ.
    Diabetes & Metabolism 03/2014; 40:A3–A4. DOI:10.1016/S1262-3636(14)72187-1 · 2.85 Impact Factor
  • Diabetes & Metabolism 03/2014; 40:A88. DOI:10.1016/S1262-3636(14)72548-0 · 2.85 Impact Factor
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    ABSTRACT: Introduction Une association inverse entre le contenu en lipides intramyocellulaires et la sensibilité à l’insuline existe chez les sujets sédentaires. Cette relation disparait chez des individus entraînés en endurance et réfère au paradoxe des athlètes. Une dérégulation de l’expression des lipases musculaire pourrait contribuer à l’insulino-résistance. L’objectif de ce travail était d’étudier l’association entre contenu en lipides intramyocellulaires, expression des lipases, capacité oxydative et sensibilité à l’insuline chez des sédentaires, des athlètes et des obèses intolérants au glucose avant et après perte de poids. Matériels et méthodes Nous avons étudié des sujets de poids normal sédentaires et entraînés en endurance, ainsi que des obèses intolérants au glucose avant et après perte de poids induite par un régime hypocalorique. La sensibilité à l’insuline a été évaluée par clamp hyperinsulinémique-euglycémique, les triacylglycérols et diacylglycérols ont été mesurés par chromatographie gazeuse. L’expression des lipases a été étudiée par Western-blot et la capacité oxydative évaluée par mesure de l’activité citrate synthase. Résultats Nos données montrent une forte association entre la sensibilité à l’insuline, la capacité oxydative et l’expression des lipases. Ces trois paramètres sont augmentés chez les athlètes et diminués chez les obèses comparés aux sédentaires. Nous observons une dissociation entre contenu en lipides intramyocellulaires toxiques et sensibilité à l’insuline avec une augmentation du contenu en diacylglycérols à la fois chez l’obèse et chez l’athlète. Nous observons également une diminution nette des triacylglycérols et diacylglycérols et de l’expression des lipases après perte de poids chez les obèses. Ces changements interviennent vis-à-vis d’une amélioration de la sensibilité à l’insuline et sans modification de la capacité oxydative musculaire. Conclusion Ces résultats suggèrent que les lipides intramyocellulaires totaux, l’expression des lipases et la capacité oxydative musculaire ne sont pas systématiquement associés, et ne constituent donc pas de bons marqueurs de la sensibilité à l’insuline.
    Diabetes & Metabolism 03/2014; 40:A11. DOI:10.1016/S1262-3636(14)72218-9 · 2.85 Impact Factor
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    ABSTRACT: Context: Soluble CD163 was suggested as a biomarker of insulin sensitivity and CD163 mRNA expression representing macrophage content in adipose tissue (AT). Objective: The aim of this study was to investigate, in cross-sectional and prospective design, the relationship between sCD163 circulating levels and, CD163 mRNA expression in adipose tissue and insulin sensitivity assessed by euglycemic-hyperinsulinemic clamp. Design, Setting, Participants, and Interventions: Two cohorts of subjects were examined in the study. Cohort 1: forty-two women with wide range of BMI (17-48 kg/m(2)); Cohort 2: twenty-seven obese women, who followed a dietary intervention consisting of 1 month very low-calorie diet, and 5 months of weight-stabilization period. Main Outcome Measures: Serum levels of CD163 and mRNA expression of CD163 and CD68 in subcutaneous and visceral AT were determined, and insulin sensitivity (expressed as glucose disposal rate (GDR)) was measured in Cohort I. In Cohort 2, serum levels of CD163, mRNA expressions of CD163, CD68, and CD163-shedding factors (TACE and TIPM3) in subcutaneous AT were examined and GDR was measured before and during dietary intervention. Results: In Cohort 1, circulating sCD163 correlated with CD163 mRNA levels in both subcutaneous and visceral AT. sCD163 and CD163 mRNA expression in both fat depots correlated with GDR. In Cohort 2, the diet-induced changes of sCD163 levels did not correlate with those of CD163, CD 68, TACE and TIMP3 mRNA levels. Although the pattern of the diet-induced change of sCD163 paralleled that of GDR there was no correlation between the changes of these two variables. Conclusion: sCD163 correlates with CD163 mRNA expression in subcutaneous and visceral AT and with whole-body insulin sensitivity in steady state condition. These associations are not observed in respect to the diet-induced changes during weight-reducing hypocaloric diet.
    The Journal of Clinical Endocrinology and Metabolism 01/2014; 99(3):jc20133348. DOI:10.1210/jc.2013-3348 · 6.31 Impact Factor
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    ABSTRACT: The aim of the present study was to investigate the influence of substrate availability on fuel selection during exercise. Eight endurance-trained male cyclists performed 90-min exercise at 70 % of their maximal oxygen uptake in a cross-over design, either in rested condition (CON) or the day after 2-h exercise practised at 70 % of maximal oxygen uptake (EX). Subjects were given a sucrose load (0.75 g kg(-1) body weight) 45 min after the beginning of the 90-min exercise test. Lipolysis was measured in subcutaneous abdominal adipose tissue (SCAT) by microdialysis and substrate oxidation by indirect calorimetry. Lipid oxidation increased during exercise and tended to decrease during sucrose ingestion in both conditions. Lipid oxidation was higher during the whole experimental period in the EX group (p = 0.004). Interestingly, fuel selection, assessed by the change in respiratory exchange ratio (RER), was increased in the EX session (p = 0.002). This was paralleled by a higher rate of SCAT lipolysis reflected by dialysate glycerol, plasma glycerol, and fatty acids (FA) levels (p < 0.001). Of note, we observed a significant relationship between whole-body fat oxidation and dialysate glycerol in both sessions (r (2) = 0.33, p = 0.02). In conclusion, this study highlights the limiting role of lipolysis and plasma FA availability to whole-body fat oxidation during exercise in endurance-trained subjects. This study shows that adipose tissue lipolysis is a determinant of fuel selection during exercise in healthy subjects.
    Journal of physiology and biochemistry 12/2013; DOI:10.1007/s13105-013-0306-z · 2.50 Impact Factor

Publication Stats

10k Citations
1,519.66 Total Impact Points

Institutions

  • 1989–2015
    • Paul Sabatier University - Toulouse III
      • • Institut des Maladies Métaboliques et Cardiovasculaires de Toulouse - UMRS 1048 - I2MC
      • • Faculté de médecine Purpan
      Tolosa de Llenguadoc, Midi-Pyrénées, France
  • 1999–2014
    • University of Toulouse
      Tolosa de Llenguadoc, Midi-Pyrénées, France
  • 1997–2014
    • Charles University in Prague
      • • 3rd Faculty of Medicine
      • • Department of Sport Medicine (3. LF)
      Praha, Praha, Czech Republic
    • Laval University
      • Département de Médecine
      Québec, Quebec, Canada
  • 1992–2014
    • French Institute of Health and Medical Research
      • Institute of Metabolic and Cardiovascular Diseases I2MC
      Lutetia Parisorum, Île-de-France, France
  • 2013
    • Telecommunications for Space and Aeronautics
      Tolosa de Llenguadoc, Midi-Pyrénées, France
  • 2010
    • Maastricht Universitair Medisch Centrum
      • Central Diagnostic Laboratory
      Maestricht, Limburg, Netherlands
  • 1990–2009
    • Unité Inserm U1077
      Caen, Lower Normandy, France
  • 2005–2007
    • Maastricht University
      • Humane Biologie
      Maastricht, Provincie Limburg, Netherlands
    • University of Geneva
      Genève, Geneva, Switzerland
    • Washington University in St. Louis
      • Department of Chemistry
      San Luis, Missouri, United States
  • 2004–2007
    • Centre Hospitalier Universitaire de Toulouse
      Tolosa de Llenguadoc, Midi-Pyrénées, France
    • Université de Rennes 1
      Roazhon, Brittany, France
  • 2004–2005
    • Stanford University
      Palo Alto, California, United States
  • 2002
    • University of Antwerp
      Antwerpen, Flanders, Belgium
  • 1992–2002
    • Lund University
      • • Department of Biophysical Chemistry
      • • Department of Physical Chemistry
      • • Department of Biophysical Chemistry
      Lund, Skåne, Sweden
  • 2000
    • University of Nantes
      Naoned, Pays de la Loire, France
  • 1998
    • Institut Louis Bachelier
      Lutetia Parisorum, Île-de-France, France
    • Généthon
      Évry-Petit-Bourg, Île-de-France, France
  • 1996
    • Umeå University
      Umeå, Västerbotten, Sweden
    • French National Institute for Agricultural Research
      Lutetia Parisorum, Île-de-France, France