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

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 Adip...

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Main Authors: Didier F. Pisani (Author), Rayane A. Ghandour (Author), Guillaume E. Beranger (Author), Pauline Le Faouder (Author), Jean-Claude Chambard (Author), Maude Giroud (Author), Alexandros Vegiopoulos (Author), Mansour Djedaini (Author), Justine Bertrand-Michel (Author), Michel Tauc (Author), Stephan Herzig (Author), Dominique Langin (Author), Gérard Ailhaud (Author), Christophe Duranton (Author), Ez-Zoubir Amri (Author)
Format: Book
Published: Elsevier, 2014-12-01T00:00:00Z.
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Summary: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.
Item Description:2212-8778
10.1016/j.molmet.2014.09.003