Suppressive actions of eicosapentaenoic acid on lipid droplet formation in 3T3-L1 adipocytes

Abstract

BackgroundLipid droplet (LD) formation and size regulation reflects both lipid influx and efflux, and is central in the regulation of adipocyte metabolism, including adipokine secretion. The length and degree of dietary fatty acid (FA) unsaturation is implicated in LD formation and regulation in adipocytes. The aims of this study were to establish the impact of eicosapentaenoic acid (EPA; C20:5n-3) in comparison to SFA (STA; stearic acid, C18:0) and MUFA (OLA; oleic acid, C18:1n-9) on 3T3-L1 adipocyte LD formation, regulation of genes central to LD function and adipokine responsiveness. Cells were supplemented with 100 μM FA during 7-day differentiation.ResultsEPA markedly reduced LD size and total lipid accumulation, suppressing PPARγ, Cidea and D9D/SCD1 genes, distinct from other treatments. These changes were independent of alterations of lipolytic genes, as both EPA and STA similarly elevated LPL and HSL gene expressions. In response to acute lipopolysaccharide exposure, EPA-differentiated adipocytes had distinct improvement in inflammatory response shown by reduction in monocyte chemoattractant protein-1 and interleukin-6 and elevation in adiponectin and leptin gene expressions.ConclusionsThis study demonstrates that EPA differentially modulates adipogenesis and lipid accumulation to suppress LD formation and size. This may be due to suppressed gene expression of key proteins closely associated with LD function. Further analysis is required to determine if EPA exerts a similar influence on LD formation and regulation in-vivo.

Docosapentaenoic acid (22:5n-3) down-regulates the expression of genes involved in fat synthesis in liver cells

“…It has been reported that EPA and DHA inhibit SREBP-1c gene transcription, enhance SREBP-1c mRNA turnover and interfere with the proteolysis processing of SREBP-1c protein (11,12). Furthermore, in another key tissue concerned with whole body lipid metabolism, it has been shown using the in vitro cell model 3T3-L1 adipocytes that EPA suppresses lipid droplet formation by suppression of the expression levels of genes related with lipid droplet function such as Cidea and Stearoyl-CoA Desaturases (13). To date, there is no data available on the effect of DPA on gene or protein expression levels of the main upstream controller of lipogenic genes, SREBP-1c.…”

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“…En el caso de la diabetes tipo 2 y el síndrome metabólico, en animales de laboratorio se ha mostrado que la suplementación con DHA y EPA mejora parámetros metabólicos como la glucosa, insulina, colesterol, lipoproteínas de baja densidad y triglicéridos en sangre (17,18). Además presentan una disminución en el tamaño de los adipocitos, y el aumento en la expresión de genes de vías como la lipolisis (degradación de los ácidos grasos) y β-oxidación (conversión de los ácidos grasos en energía) en este mismo tejido (19,20).…”

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“…En estudios sobre esteatosis hepática, se descubrió que el EPA disminuye la esteatosis de manera independiente a su interacción con el PPAR-α, esto se traduce en una menor captación de ácidos grasos y una mayor hidrólisis de triglicéridos intrahepáticos (41). El EPA modula diferencialmente la adipogénesis y reduce el tamaño de la gota lipídica en los adipocitos, debido a que disminuye la expresión del PPAR-γ (42), y aumenta la expresión del gen de la enzima lipasa hormona sensible, lo que acelera la movilización de triglicéridos desde los adipocitos (42). Esto se traduce en una menor formación de adipocitos y en un menor contenido de grasa en ellos (42).…”