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Pisani, D.F.* ; Ghandour, R.A.* ; Beranger, G.E.* ; Le Faouder, P.* ; Chambard, J.C.* ; Giroud, M.* ; Vegiopoulos, A.* ; Djedaini, M.* ; Bertrand-Michel, J.* ; Tauc, M.* ; Herzig, S.* ; Langin, D.* ; Ailhaud, G.* ; Duranton, C.* ; Amri, E.Z.*

The ω6-fatty acid, arachidonic acid, regulates the conversion of white to brite adipocyte through a prostaglandin/calcium mediated pathway.

Mol. Metab. 3, 834-847 (2014)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
OBJECTIVE: 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. METHODS/RESULTS: 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. CONCLUSION: 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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Calcium Oscillation ; Pge2 ; Pgf2α ; Pgi2 ; Polyunsaturated Fatty Acids ; Ucp1
Sprache englisch
Veröffentlichungsjahr 2014
HGF-Berichtsjahr 0
ISSN (print) / ISBN 2212-8778
e-ISSN 2212-8778
Zeitschrift Molecular Metabolism
Quellenangaben Band: 3, Heft: 9, Seiten: 834-847 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort Amsterdam
Begutachtungsstatus Peer reviewed
PubMed ID 25506549
Erfassungsdatum 2014-12-31