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  1. Article ; Online: The timing of eating controls energy use.

    Lagarde, Damien / Kazak, Lawrence

    Science (New York, N.Y.)

    2022  Volume 378, Issue 6617, Page(s) 251–252

    Abstract: Synchronizing food intake with the body clock boosts thermogenesis and limits obesity. ...

    Abstract Synchronizing food intake with the body clock boosts thermogenesis and limits obesity.
    MeSH term(s) Humans ; Eating ; Energy Intake ; Energy Metabolism ; Obesity/prevention & control ; Thermogenesis ; Circadian Clocks
    Language English
    Publishing date 2022-10-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.ade6720
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  2. Article ; Online: Creatine promotes metastatic dissemination.

    Lagarde, Damien / Kazak, Lawrence

    Cell metabolism

    2021  Volume 33, Issue 6, Page(s) 1065–1067

    Abstract: The molecular regulation of cancer metastasis is not fully understood. In this issue of Cell Metabolism, Zhang et al. (2021) discover that creatine promotes cancer metastasis in mice by promoting activation of the MPS1-Smad2/3 axis. ...

    Abstract The molecular regulation of cancer metastasis is not fully understood. In this issue of Cell Metabolism, Zhang et al. (2021) discover that creatine promotes cancer metastasis in mice by promoting activation of the MPS1-Smad2/3 axis.
    MeSH term(s) Animals ; Creatine ; Mice ; Neoplasms
    Chemical Substances Creatine (MU72812GK0)
    Language English
    Publishing date 2021-06-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2021.05.012
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  3. Article ; Online: Parallel control of cold-triggered adipocyte thermogenesis by UCP1 and CKB.

    Rahbani, Janane F / Bunk, Jakub / Lagarde, Damien / Samborska, Bozena / Roesler, Anna / Xiao, Haopeng / Shaw, Abhirup / Kaiser, Zafir / Braun, Jessica L / Geromella, Mia S / Fajardo, Val A / Koza, Robert A / Kazak, Lawrence

    Cell metabolism

    2024  Volume 36, Issue 3, Page(s) 526–540.e7

    Abstract: That uncoupling protein 1 (UCP1) is the sole mediator of adipocyte thermogenesis is a conventional viewpoint that has primarily been inferred from the attenuation of the thermogenic output of mice genetically lacking Ucp1 from birth (germline ... ...

    Abstract That uncoupling protein 1 (UCP1) is the sole mediator of adipocyte thermogenesis is a conventional viewpoint that has primarily been inferred from the attenuation of the thermogenic output of mice genetically lacking Ucp1 from birth (germline Ucp1
    MeSH term(s) Animals ; Mice ; Adipocytes, Brown/metabolism ; Adipose Tissue, Brown/metabolism ; Thermogenesis ; Uncoupling Protein 1/genetics ; Uncoupling Protein 1/metabolism ; Creatine Kinase, BB Form/metabolism
    Chemical Substances Uncoupling Protein 1 ; Creatine Kinase, BB Form (EC 2.7.3.2) ; Ucp1 protein, mouse
    Language English
    Publishing date 2024-01-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2024.01.001
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  4. Article: Lactate Fluxes and Plasticity of Adipose Tissues: A Redox Perspective.

    Lagarde, Damien / Jeanson, Yannick / Portais, Jean-Charles / Galinier, Anne / Ader, Isabelle / Casteilla, Louis / Carrière, Audrey

    Frontiers in physiology

    2021  Volume 12, Page(s) 689747

    Abstract: Lactate, a metabolite produced when the glycolytic flux exceeds mitochondrial oxidative capacities, is now viewed as a critical regulator of metabolism by acting as both a carbon and electron carrier and a signaling molecule between cells and tissues. In ...

    Abstract Lactate, a metabolite produced when the glycolytic flux exceeds mitochondrial oxidative capacities, is now viewed as a critical regulator of metabolism by acting as both a carbon and electron carrier and a signaling molecule between cells and tissues. In recent years, increasing evidence report its key role in white, beige, and brown adipose tissue biology, and highlights new mechanisms by which lactate participates in the maintenance of whole-body energy homeostasis. Lactate displays a wide range of biological effects in adipose cells not only through its binding to the membrane receptor but also through its transport and the subsequent effect on intracellular metabolism notably on redox balance. This study explores how lactate regulates adipocyte metabolism and plasticity by balancing intracellular redox state and by regulating specific signaling pathways. We also emphasized the contribution of adipose tissues to the regulation of systemic lactate metabolism, their roles in redox homeostasis, and related putative physiopathological repercussions associated with their decline in metabolic diseases and aging.
    Language English
    Publishing date 2021-06-30
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2021.689747
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  5. Article ; Online: The emerging roles of lactate as a redox substrate and signaling molecule in adipose tissues.

    Carrière, Audrey / Lagarde, Damien / Jeanson, Yannick / Portais, Jean-Charles / Galinier, Anne / Ader, Isabelle / Casteilla, Louis

    Journal of physiology and biochemistry

    2020  Volume 76, Issue 2, Page(s) 241–250

    Abstract: Thermogenic (brown and beige) adipose tissues improve glucose and lipid homeostasis and therefore represent putative targets to cure obesity and related metabolic diseases including type II diabetes. Beside decades of research and the very well-described ...

    Abstract Thermogenic (brown and beige) adipose tissues improve glucose and lipid homeostasis and therefore represent putative targets to cure obesity and related metabolic diseases including type II diabetes. Beside decades of research and the very well-described role of noradrenergic signaling, mechanisms underlying adipocytes plasticity and activation of thermogenic adipose tissues remain incompletely understood. Recent studies show that metabolites such as lactate control the oxidative capacity of thermogenic adipose tissues. Long time viewed as a metabolic waste product, lactate is now considered as an important metabolic substrate largely feeding the oxidative metabolism of many tissues, acting as a signaling molecule and as an inter-cellular and inter-tissular redox carrier. In this review, we provide an overview of the recent findings highlighting the importance of lactate in adipose tissues, from its production to its role as a browning inducer and its metabolic links with brown adipose tissue. We also discuss additional function(s) than thermogenesis ensured by brown and beige adipose tissues, i.e., their ability to dissipate high redox pressure and oxidative stress thanks to the activity of the uncoupling protein-1, helping to maintain tissue and whole organism redox homeostasis and integrity.
    MeSH term(s) Adipose Tissue, Beige/cytology ; Adipose Tissue, Beige/metabolism ; Adipose Tissue, Brown/cytology ; Adipose Tissue, Brown/metabolism ; Animals ; Energy Metabolism ; Humans ; Lactic Acid/metabolism ; Oxidation-Reduction ; Oxidative Stress ; Thermogenesis ; Uncoupling Protein 1/metabolism
    Chemical Substances UCP1 protein, human ; Uncoupling Protein 1 ; Lactic Acid (33X04XA5AT)
    Language English
    Publishing date 2020-01-02
    Publishing country Spain
    Document type Journal Article ; Review
    ZDB-ID 1325104-1
    ISSN 1877-8755 ; 0034-9402 ; 1138-7548
    ISSN (online) 1877-8755
    ISSN 0034-9402 ; 1138-7548
    DOI 10.1007/s13105-019-00723-2
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  6. Article ; Online: CD36 Drives Metastasis and Relapse in Acute Myeloid Leukemia.

    Farge, Thomas / Nakhle, Jean / Lagarde, Damien / Cognet, Guillaume / Polley, Nathaniel / Castellano, Rémy / Nicolau, Marie-Laure / Bosc, Claudie / Sabatier, Marie / Sahal, Ambrine / Saland, Estelle / Jeanson, Yannick / Guiraud, Nathan / Boet, Emeline / Bergoglio, Camille / Gotanègre, Mathilde / Mouchel, Pierre-Luc / Stuani, Lucille / Larrue, Clément /
    Sallese, Marie / De Mas, Véronique / Moro, Cedric / Dray, Cédric / Collette, Yves / Raymond-Letron, Isabelle / Ader, Isabelle / Récher, Christian / Sarry, Jean-Emmanuel / Cabon, Florence / Vergez, François / Carrière, Audrey

    Cancer research

    2023  Volume 83, Issue 17, Page(s) 2824–2838

    Abstract: Identifying mechanisms underlying relapse is a major clinical issue for effective cancer treatment. The emerging understanding of the importance of metastasis in hematologic malignancies suggests that it could also play a role in drug resistance and ... ...

    Abstract Identifying mechanisms underlying relapse is a major clinical issue for effective cancer treatment. The emerging understanding of the importance of metastasis in hematologic malignancies suggests that it could also play a role in drug resistance and relapse in acute myeloid leukemia (AML). In a cohort of 1,273 AML patients, we uncovered that the multifunctional scavenger receptor CD36 was positively associated with extramedullary dissemination of leukemic blasts, increased risk of relapse after intensive chemotherapy, and reduced event-free and overall survival. CD36 was dispensable for lipid uptake but fostered blast migration through its binding with thrombospondin-1. CD36-expressing blasts, which were largely enriched after chemotherapy, exhibited a senescent-like phenotype while maintaining their migratory ability. In xenograft mouse models, CD36 inhibition reduced metastasis of blasts and prolonged survival of chemotherapy-treated mice. These results pave the way for the development of CD36 as an independent marker of poor prognosis in AML patients and a promising actionable target to improve the outcome of patients.
    Significance: CD36 promotes blast migration and extramedullary disease in acute myeloid leukemia and represents a critical target that can be exploited for clinical prognosis and patient treatment.
    MeSH term(s) Humans ; Animals ; Mice ; Leukemia, Myeloid, Acute/pathology ; Treatment Outcome ; Prognosis ; Recurrence ; Blast Crisis/pathology ; Chronic Disease
    Language English
    Publishing date 2023-06-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-22-3682
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  7. Article ; Online: Lactate fluxes mediated by the monocarboxylate transporter-1 are key determinants of the metabolic activity of beige adipocytes.

    Lagarde, Damien / Jeanson, Yannick / Barreau, Corinne / Moro, Cedric / Peyriga, Lindsay / Cahoreau, Edern / Guissard, Christophe / Arnaud, Emmanuelle / Galinier, Anne / Bouzier-Sore, Anne-Karine / Pellerin, Luc / Chouchani, Edward T / Pénicaud, Luc / Ader, Isabelle / Portais, Jean-Charles / Casteilla, Louis / Carrière, Audrey

    The Journal of biological chemistry

    2020  Volume 296, Page(s) 100137

    Abstract: Activation of energy-dissipating brown/beige adipocytes represents an attractive therapeutic strategy against metabolic disorders. While lactate is known to induce beiging through the regulation of Ucp1 gene expression, the role of lactate transporters ... ...

    Abstract Activation of energy-dissipating brown/beige adipocytes represents an attractive therapeutic strategy against metabolic disorders. While lactate is known to induce beiging through the regulation of Ucp1 gene expression, the role of lactate transporters on beige adipocytes' ongoing metabolic activity remains poorly understood. To explore the function of the lactate-transporting monocarboxylate transporters (MCTs), we used a combination of primary cell culture studies,
    MeSH term(s) Adipocytes, Beige/cytology ; Adipocytes, Beige/metabolism ; Animals ; Gene Expression Regulation ; Lactic Acid/metabolism ; Male ; Mesenchymal Stem Cells/cytology ; Mesenchymal Stem Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Monocarboxylic Acid Transporters/genetics ; Monocarboxylic Acid Transporters/metabolism ; Signal Transduction ; Symporters/genetics ; Symporters/metabolism ; Thermogenesis
    Chemical Substances Monocarboxylic Acid Transporters ; Symporters ; monocarboxylate transport protein 1 ; Lactic Acid (33X04XA5AT)
    Language English
    Publishing date 2020-12-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.RA120.016303
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  8. Article ; Online: ADRA1A-Gα

    Rahbani, Janane F / Scholtes, Charlotte / Lagarde, Damien M / Hussain, Mohammed F / Roesler, Anna / Dykstra, Christien B / Bunk, Jakub / Samborska, Bozena / O'Brien, Shannon L / Tripp, Emma / Pacis, Alain / Angueira, Anthony R / Johansen, Olivia S / Cinkornpumin, Jessica / Hossain, Ishtiaque / Lynes, Matthew D / Zhang, Yang / White, Andrew P / Pastor, William A /
    Chondronikola, Maria / Sidossis, Labros / Klein, Samuel / Kralli, Anastasia / Cypess, Aaron M / Pedersen, Steen B / Jessen, Niels / Tseng, Yu-Hua / Gerhart-Hines, Zachary / Seale, Patrick / Calebiro, Davide / Giguère, Vincent / Kazak, Lawrence

    Nature metabolism

    2022  Volume 4, Issue 11, Page(s) 1459–1473

    Abstract: Noradrenaline (NA) regulates cold-stimulated adipocyte ... ...

    Abstract Noradrenaline (NA) regulates cold-stimulated adipocyte thermogenesis
    MeSH term(s) Creatine/metabolism ; Thermogenesis/genetics ; Adipocytes/metabolism ; Energy Metabolism/genetics ; Creatine Kinase/metabolism
    Chemical Substances Creatine (MU72812GK0) ; Creatine Kinase (EC 2.7.3.2)
    Language English
    Publishing date 2022-11-07
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-022-00667-w
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  9. Article ; Online: Atrial Natriuretic Peptide Orchestrates a Coordinated Physiological Response to Fuel Non-shivering Thermogenesis.

    Carper, Deborah / Coué, Marine / Nascimento, Emmani B M / Barquissau, Valentin / Lagarde, Damien / Pestourie, Carine / Laurens, Claire / Petit, Justine Vily / Soty, Maud / Monbrun, Laurent / Marques, Marie-Adeline / Jeanson, Yannick / Sainte-Marie, Yannis / Mairal, Aline / Déjean, Sébastien / Tavernier, Geneviève / Viguerie, Nathalie / Bourlier, Virginie / Lezoualc'h, Frank /
    Carrière, Audrey / Saris, Wim H M / Astrup, Arne / Casteilla, Louis / Mithieux, Gilles / van Marken Lichtenbelt, Wouter / Langin, Dominique / Schrauwen, Patrick / Moro, Cedric

    Cell reports

    2020  Volume 32, Issue 8, Page(s) 108075

    Abstract: Atrial natriuretic peptide (ANP) is a cardiac hormone controlling blood volume and pressure in mammals. It is still unclear whether ANP controls cold-induced thermogenesis in vivo. Here, we show that acute cold exposure induces cardiac ANP secretion in ... ...

    Abstract Atrial natriuretic peptide (ANP) is a cardiac hormone controlling blood volume and pressure in mammals. It is still unclear whether ANP controls cold-induced thermogenesis in vivo. Here, we show that acute cold exposure induces cardiac ANP secretion in mice and humans. Genetic inactivation of ANP promotes cold intolerance and suppresses half of cold-induced brown adipose tissue (BAT) activation in mice. While white adipocytes are resistant to ANP-mediated lipolysis at thermoneutral temperature in mice, cold exposure renders white adipocytes fully responsive to ANP to activate lipolysis and a thermogenic program, a physiological response that is dramatically suppressed in ANP null mice. ANP deficiency also blunts liver triglycerides and glycogen metabolism, thus impairing fuel availability for BAT thermogenesis. ANP directly increases mitochondrial uncoupling and thermogenic gene expression in human white and brown adipocytes. Together, these results indicate that ANP is a major physiological trigger of BAT thermogenesis upon cold exposure in mammals.
    Language English
    Publishing date 2020-08-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2020.108075
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