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Eicosapentaenoic acid up‐regulates apelin secretion and gene expression in 3T3‐L1 adipocytes
Author(s) -
LorenteCebrián Silvia,
Bustos Matilde,
Marti Amelia,
Martinez José Alfredo,
MorenoAliaga María Jesús
Publication year - 2010
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200900522
Subject(s) - apelin , endocrinology , medicine , eicosapentaenoic acid , secretion , biology , pi3k/akt/mtor pathway , cycloheximide , chemistry , polyunsaturated fatty acid , fatty acid , microbiology and biotechnology , biochemistry , signal transduction , receptor , protein biosynthesis
Recent studies have shown the ability of apelin to restore glucose tolerance in obese and insulin‐resistant mice. Eicosapentaenoic acid (EPA) is a polyunsaturated fatty acid (PUFA) from the omega‐3 family that has many beneficial effects in obesity‐linked disorders. The aim of this study was to examine in vitro the effects of EPA on apelin secretion and gene expression in mature 3T3‐L1 adipocytes. Treatment with EPA (100 and 200 μM) significantly increased basal ( p <0.01) and insulin‐stimulated ( p <0.001) apelin secretion and gene expression in adipocytes. EPA also stimulated Akt phosphorylation, a down‐stream target of phosphatidylinositol 3‐kinase (PI3K), in 3T3‐L1 adipocytes. Moreover, treatment with the PI3K inhibitor LY294002 completely blocked EPA‐stimulatory action on apelin mRNA gene expression ( p <0.001), but not modified the stimulatory effect of EPA on basal apelin secretion. Furthermore, the stimulatory effect of EPA on basal apelin release was also observed in the presence of Actinomycin D and Cycloheximide, suggesting that EPA might also regulate apelin secretion by via post‐transcriptional mechanisms. These findings suggest that the mechanisms mediating EPA‐induced apelin synthesis and/or secretion are complex, involving steps that are PI3K dependent and steps that are PI3K independent.