Molecular Nutrition Unit, School of Exercise and Nutrition Sciences, Faculty of Health, Medicine, Nursing and Behavioural Sciences, Deakin University, Melbourne, Victoria, Australia.
Lipids Health Dis. 2010 Jun 4;9:57. doi: 10.1186/1476-511X-9-57.
Lipid 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 microM FA during 7-day differentiation.
EPA markedly reduced LD size and total lipid accumulation, suppressing PPARgamma, 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.
This 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.
脂滴 (LD) 的形成和大小调节反映了脂质的流入和流出,是调节脂肪细胞代谢的核心,包括脂肪因子的分泌。脂肪酸 (FA) 的长度和不饱和程度与脂肪细胞中 LD 的形成和调节有关。本研究的目的是确定二十碳五烯酸 (EPA; C20:5n-3) 与饱和脂肪酸 (STA; 硬脂酸,C18:0) 和单不饱和脂肪酸 (OLA; 油酸,C18:1n-9) 对 3T3-L1 脂肪细胞 LD 形成、LD 功能和脂肪因子反应相关基因的调控的影响。细胞在分化的第 7 天用 100 μM FA 补充。
EPA 显著降低了 LD 大小和总脂质积累,抑制了 PPARγ、Cidea 和 D9D/SCD1 基因,与其他处理不同。这些变化与脂解基因的改变无关,因为 EPA 和 STA 同样增加了 LPL 和 HSL 基因的表达。急性脂多糖暴露后,EPA 分化的脂肪细胞表现出明显改善的炎症反应,单核细胞趋化蛋白-1 和白细胞介素-6 减少,而脂联素和瘦素基因表达增加。
本研究表明,EPA 可调节脂肪生成和脂质积累,从而抑制 LD 的形成和大小。这可能是由于与 LD 功能密切相关的关键蛋白的基因表达受到抑制。需要进一步分析以确定 EPA 是否对体内 LD 的形成和调节有类似的影响。