Fig. 6.

EPA competes with ARA at the cyclooxygenase level. hMADS cells were differentiated into white or brite adipocytes. A: Brite hMADS adipocytes were treated with 10 nM fluprostenol (agonist of PGF2α receptor) in the presence or absence of 3.3 µM EPA during the last 3 days of adipogenic differentiation. UCP1 and PLN1 were evaluated by RT-qPCR. B: Brite hMADS were exposed to 10 µM ARA in the presence or absence of 3.3 µM EPA for 1 or 24 h. PGF2α was quantified in culture media by Elisa Immuno Assay. C: Brite hMADS adipocytes were treated with 10 µM ARA in the presence or absence of 3.3 µM EPA during the last 3 days of differentiation. Expression of enzymes involved in the metabolization of ARA to PGF2α was evaluated by RT-qPCR. mRNA expressions are expressed as fold increase relative to “brite” values. Data are mean ± SEM of 3 independent experiments. a, P < 0.01 versus brite; b, P < 0.01 versus brite + ARA.