首页> 外文期刊>Lipids in Health Disease >Suppressive actions of eicosapentaenoic acid on lipid droplet formation in 3T3-L1 adipocytes
【24h】

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

机译:二十碳五烯酸对3T3-L1脂肪细胞脂质滴形成的抑制作用

获取原文
获取外文期刊封面目录资料

摘要

Background 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 μM FA during 7-day differentiation. Results EPA 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. Conclusions 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.
机译:背景脂质小滴(LD)的形成和大小的调节既反映了脂质的流入和流出,又是调节脂肪细胞代谢(包括脂肪因子分泌)的关键。膳食脂肪酸(FA)不饱和的长度和程度与脂肪细胞中LD的形成和调节有关。这项研究的目的是确定二十碳五烯酸(EPA; C20:5n-3)与SFA(STA;硬脂酸,C18:0)和MUFA(OLA;油酸,C18:1n-9)的影响对3T3-L1脂肪细胞LD形成,LD功能关键基因和脂肪因子反应性的调节。在7天的分化过程中向细胞补充了100μMFA。结果EPA明显减少了LD的大小和总脂质积累,抑制了PPARγ,Cidea和D9D / SCD1基因,这与其他治疗方法不同。这些变化与脂解基因的改变无关,因为EPA和STA都类似地提高了LPL和HSL基因的表达。针对急性脂多糖暴露,EPA分化的脂肪细胞在炎症反应方面有明显改善,表现为单核细胞趋化蛋白-1和白介素-6减少以及脂联素和瘦素基因表达升高。结论这项研究表明,EPA差异性调节脂肪形成和脂质积聚,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LD的体内形成和调节产生类似的影响。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号