Ntambi J M, Bené H
Department of Biochemistry, University of Wisconsin-Madison, 53706-1544, USA.
J Mol Neurosci. 2001 Apr-Jun;16(2-3):273-8; discussion 279-84. doi: 10.1385/JMN:16:2-3:273.
Polyunsaturated fatty acids (PUFAs), specifically the n-3 and n-6 series, play a key role in the progression or prevention of human diseases such as obesity, diabetes, cancer, neurological and heart disease, mainly by affecting cellular membrane lipid composition, metabolism, signal-transduction pathways, and by direct control of gene expression. PUFAs show regulation of gene expression in several tissues, including brain, liver, heart, and adipose. Most recently, research has focused on identifying the mechanisms by which PUFAs regulate lipogenic gene expression. Research to date indicates that PUFA-mediated regulation of the genetic expression and proteolytic maturation of a group of transcription factors termed sterol regulatory element binding proteins (SREBPs) accounts for the suppression of hepatic lipogenic gene expression. However, our recent studies on the transcriptional regulation of the stearoyl-coenzyme A (CoA) desaturase gene, encoding a key enzyme in the cellular synthesis of monounsaturated fatty acids from saturated fatty acids indicates that PUFA can suppress gene transcription by a mechanism independent of SREBP maturation.
多不饱和脂肪酸(PUFAs),特别是n-3和n-6系列,在人类疾病如肥胖症、糖尿病、癌症、神经系统疾病和心脏病的发展或预防中起着关键作用,主要是通过影响细胞膜脂质组成、代谢、信号转导途径以及直接控制基因表达来实现的。PUFAs在包括脑、肝、心脏和脂肪组织在内的多种组织中显示出对基因表达的调节作用。最近,研究集中在确定PUFAs调节脂肪生成基因表达的机制上。迄今为止的研究表明,PUFA介导的对一组称为固醇调节元件结合蛋白(SREBPs)的转录因子的基因表达和蛋白水解成熟的调节,是肝脏脂肪生成基因表达受到抑制的原因。然而,我们最近对硬脂酰辅酶A(CoA)去饱和酶基因转录调控的研究表明,该基因编码一种将饱和脂肪酸转化为单不饱和脂肪酸的细胞合成关键酶,PUFA可通过一种独立于SREBP成熟的机制抑制基因转录。