Arachidonic acid maldistribution in obesity

Arachidonic acid maldistribution in obesity
复制标题

DOI:
10.1007/bf02637089
复制
发表时间:
2007
期刊:
影响因子:
1.9
通讯作者:
S. Phinney
S. Phinney
中科院分区:
医学4区
文献类型:
--
作者:
S. Phinney

文献摘要

被引文献

相似文献

花生四烯酸是细胞功能的重要调节剂,其以游离形式或作为类二十烷酸的底物对细胞膜的物理性质产生影响。饮食研究表明其生产受到调节,但这种调节的机制和影响花生四烯酸在生产地点分布的因素仍有待确定。特别是,花生四烯酸从磷脂中释放后是否具有非氧化命运尚未确定。血清、肝脏和肌肉脂质部分的花生四烯酸含量的变化与脂肪生成和胰岛素作用的改变相关,这意味着花生四烯酸在燃料分配中的作用。在啮齿动物和人类的肥胖遗传模型中已经发现了这种机制发挥系统作用的证据。本综述提出,磷脂和胆固醇酯部分之间花生四烯酸分布的变化参与了与某些形式的遗传性肥胖相关的异常燃料分配。
Arachidonic acid is an important regulator of cellular function via its effects on the physical properties of membranes, in its free form, or as a substrate for eicosanoids. Dietary studies indicate that its production is regulated, but the mechanisms of this regulation and factors influencing arachidonate distribution from the site of production remain to be determined. In particular, whether there is a nonoxidative fate for arachidonate once it has been released from phospholipid has yet to be determined. Variations in the arachidonate content of serum, liver, and muscle lipid fractions have been correlated with alterations in lipogenesis and insulin action, implying a role for arachidonate in fuel partitioning. Evidence for this mechanism acting systemically has been found in genetic models of obesity in rodents and also in humans. This review proposes that variation in the distribution of arachidonate between phospholipid and cholesteryl ester fractions participates in the abnormal fuel partitioning associated with some forms of genetic obesity.