Pisani Didier F, Ghandour Rayane A, Beranger Guillaume E, Le Faouder Pauline, Chambard Jean-Claude, Giroud Maude, Vegiopoulos Alexandros, Djedaini Mansour, Bertrand-Michel Justine, Tauc Michel, Herzig Stephan, Langin Dominique, Ailhaud Gérard, Duranton Christophe, Amri Ez-Zoubir
Univ. Nice Sophia Antipolis, iBV, UMR 7277, 06100 Nice, France ; CNRS, iBV, UMR 7277, 06100 Nice, France ; Inserm, iBV, U1091, 06100 Nice, France.
Lipidomic Core Facility, Metatoul Platform, France ; INSERM, UMR1048, Obesity Research Laboratory, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France ; University of Toulouse, UMR1048, Paul Sabatier University, Toulouse, France.
Mol Metab. 2014 Sep 16;3(9):834-47. doi: 10.1016/j.molmet.2014.09.003. eCollection 2014 Dec.
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.
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.
米色脂肪细胞是可诱导的耗能细胞，表达解偶联蛋白1（UCP1），出现在健康成年个体的白色脂肪组织中。募集这些细胞是对抗肥胖及相关疾病的一种潜在策略。
方法/结果：利用能够转化为米色脂肪细胞的人多能脂肪干细胞，我们发现花生四烯酸通过环氧化酶途径强烈抑制米色脂肪细胞形成，该途径导致前列腺素E2（PGE2）和前列腺素F2α（PGF2α）的分泌。这两种前列腺素均诱导与细胞外信号调节激酶（ERK）途径偶联的振荡性钙离子信号，并触发UCP1表达及氧消耗的减少，而不改变线粒体生成。在喂食添加了ω6花生四烯酸的标准饮食的小鼠中，皮下白色脂肪组织中PGF2α和PGE2的量增加，且与米色脂肪细胞募集的减少相关。
我们的结果表明，西方饮食中过量的ω6多不饱和脂肪酸也可能通过阻止“褐变”过程的发生而促进肥胖。
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