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The authors acknowledge the staff from Auvergne University Experimental Animal Laboratory and Christophe Del’Homme, Philippe Denis, Anne Terisse-Lottier and Alexandre Teynie from the Experimental Animal Facility of the Human Nutrition Unit (INRA of Clermont-Ferrand) for their assistance throughout the animal protocol. We thank Celine Bobby for her help for TaqMan gene expression assays. We gratefully acknowledge financial support and doctoral fellowship (to A.P.) fromLesieur and AvrilImpact of ALA, EPA and DHA on obesity and metabolic complications were studied in mice fed a high-fat high-sucrose diet (HF). HF diets were supplemented with ALA, EPA or DHA (1%w/w) and given to C57BL/6J mice for 16 weeks and to Ob/Ob mice for 6 weeks. In C57BL/6J mice, EPA reduced plasma cholesterol (-20%), limited fat mass accumulation (-23%), adipose cell hypertrophy (-50%), and reduced plasma leptin concentration (-60%), compared to HF fed mice. Furthermore, mice supplemented with EPA exhibited a higher insulin sensitivity (+24%) and glucose tolerance (+20%) compared to HF fed mice. Similar effects were observed in EPA supplemented Ob/Ob mice, although fat mass accumulation was not prevented. By contrast in comparison to HF fed mice, DHA did not prevent fat mass accumulation, increased plasma leptin concentration (+128%) in C57BL/6J mice and did not improve glucose homeostasis in C57BL/6J and Ob/Ob mice. In 3T3-L1 adipocytes, DHA stimulated leptin expression whereas EPA induced adiponectin expression, suggesting that improved leptin / adiponectin balance may contribute to the protective effect of EPA. In conclusion, supplementation with EPA, but not ALA and DHA, could preserve glucose homeostasis in an obesogenic environment and limit fat mass accumulation in the early stage of weight gain