TY - JOUR
T1 - Atrial Natriuretic Peptide Orchestrates a Coordinated Physiological Response to Fuel Non-shivering Thermogenesis
AU - Carper, Deborah
AU - Coue, Marine
AU - Nascimento, Emmani B. M.
AU - Barquissau, Valentin
AU - Lagarde, Damien
AU - Pestourie, Carine
AU - Laurens, Claire
AU - Petit, Justine Vily
AU - Soty, Maud
AU - Monbrun, Laurent
AU - Marques, Marie-Adeline
AU - Jeanson, Yannick
AU - Sainte-Marie, Yannis
AU - Mairal, Aline
AU - Dejean, Sebastien
AU - Tavernier, Genevieve
AU - Viguerie, Nathalie
AU - Bourlier, Virginie
AU - Lezoualc'h, Frank
AU - Carriere, Audrey
AU - Saris, Wim H. M.
AU - Astrup, Arne
AU - Casteilla, Louis
AU - Mithieux, Gilles
AU - van Marken Lichtenbelt, W. D.
AU - Langin, Dominique
AU - Schrauwen, Patrick
AU - Moro, Cedric
N1 - Funding Information:
This work was supported by grants from INSERM , Société Francophone du Diabète , and the European Foundation for the Study of Diabetes (C.M.) and the Commission of the European Communities ( FP6-513946 DiOGenes and HEALTH-F2-2011-278373 DIABAT ) (D. Lagarde). D.C. is supported by a PhD fellowship from INSERM/Occitanie Region . We are very grateful to Caroline Nevoit, Sarah Gandarillas, and Candy Escassut (CREFRE) for technical assistance in PET/CT imaging. We also thank Alexandre Lucas (APC core facility), Frédéric Martins (GET-TQ core facility), Lucie Fontaine (Histology core facility), and Dr. Jean-Philippe Pradère and Enzo Piccolo (Liver ORO staining) for their technical support. D.L. is a member of Institut Universitaire de France. We warmly acknowledge Pr. Max Lafontan for critical reading of the manuscript.
Funding Information:
This work was supported by grants from INSERM, Soci?t? Francophone du Diab?te, and the European Foundation for the Study of Diabetes (C.M.) and the Commission of the European Communities (FP6-513946 DiOGenes and HEALTH-F2-2011-278373 DIABAT) (D. Lagarde). D.C. is supported by a PhD fellowship from INSERM/Occitanie Region. We are very grateful to Caroline Nevoit, Sarah Gandarillas, and Candy Escassut (CREFRE) for technical assistance in PET/CT imaging. We also thank Alexandre Lucas (APC core facility), Fr?d?ric Martins (GET-TQ core facility), Lucie Fontaine (Histology core facility), and Dr. Jean-Philippe Prad?re and Enzo Piccolo (Liver ORO staining) for their technical support. D.L. is a member of Institut Universitaire de France. We warmly acknowledge Pr. Max Lafontan for critical reading of the manuscript. Conceptualization, D.C. and C.M.; Methodology, D.C. and C.M.; Investigation, D.C. M.C. E.B.M.N. V.B. D.A.L. C.P. C.L. J.V.P. M.S. L.M. M.-A.M. Y.J. Y.S.-M. A.M. S.D. G.T. N.V. V.B. F.L. A.C. W.H.M.S. and A.A.; Resources, G.M. W.v.M.L. P.S. D.L.; Writing ? Original Draft, D.C. and C.M.; Writing ? Review & Editing, D.C. E.B.M.N. A.C. L.C. G.M. W.v.M.L. P.S. D.L. and C.M.; Supervision, D.C. and C.M.; Funding Acquisition, D.L. and C.M. The authors declare no competing interests.
Publisher Copyright:
© 2020 The Author(s)
PY - 2020/8/25
Y1 - 2020/8/25
N2 - 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.
AB - 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.
KW - BROWN ADIPOSE-TISSUE
KW - COLD-INDUCED THERMOGENESIS
KW - ACTIVATED PROTEIN-KINASE
KW - INSULIN-RESISTANCE
KW - BEIGE ADIPOCYTES
KW - WEIGHT-LOSS
KW - RECEPTOR
KW - OBESITY
KW - INDUCE
KW - IDENTIFICATION
U2 - 10.1016/j.celrep.2020.108075
DO - 10.1016/j.celrep.2020.108075
M3 - Article
C2 - 32846132
SN - 2211-1247
VL - 32
JO - Cell Reports
JF - Cell Reports
IS - 8
M1 - 108075
ER -