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首页> 外文期刊>Current opinion in lipidology >N-3 polyunsaturated fatty acid regulation of hepatic gene transcription.
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N-3 polyunsaturated fatty acid regulation of hepatic gene transcription.

机译：N-3多不饱和脂肪酸调节肝基因转录。

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PURPOSE OF REVIEW: The liver plays a central role in whole body lipid metabolism and adapts rapidly to changes in dietary fat composition. This adaption involves changes in the expression of genes involved in glycolysis, de-novo lipogenesis, fatty acid elongation, desaturation and oxidation. This review brings together metabolic and molecular studies that help explain n-3 (omega-3) polyunsaturated fatty acid regulation of hepatic gene transcription. RECENT FINDINGS: Dietary n-3 polyunsaturated fatty acid regulates hepatic gene expression by targeting three major transcriptional regulatory networks: peroxisome proliferator-activated receptor alpha, sterol regulatory element binding protein-1 and the carbohydrate regulatory element binding protein/Max-like factor X heterodimer. 22: 6,n-3, the most prominent n-3 polyunsaturated fatty acid in tissues, is a weak activator of peroxisome proliferator-activated receptor alpha. Hepatic metabolism of 22: 6,n-3, however, generates 20: 5,n-3, a strong peroxisome proliferator-activated receptor alpha activator. In contrast to peroxisome proliferator-activated receptor alpha, 22: 6,n-3 is the most potent fatty acid regulator of hepatic sterol regulatory element binding protein-1. 22: 6,n-3 suppresses sterol regulatory element binding protein-1 gene expression while enhancing degradation of nuclear sterol regulatory element binding protein-1 through 26S proteasome and Erk1/2-dependent mechanisms. Both n-3 and n-6 polyunsaturated fatty acid suppress carbohydrate regulatory element binding protein and Max-like factor X nuclear abundance and interfere with glucose-regulated hepatic metabolism. SUMMARY: These studies have revealed unique mechanisms by which specific polyunsaturated fatty acids control peroxisome proliferator activated receptor alpha, sterol regulatory element binding protein-1 and carbohydrate regulatory element binding protein/Max-like factor X function. As such, specific metabolic and signal transduction pathways contribute significantly to the fatty acidregulation of these transcription factors and their corresponding regulatory networks.
机译：审查目的：肝脏在全身脂质代谢中起着核心作用，并迅速适应饮食脂肪成分的变化。这种适应作用涉及糖酵解，新脂质生成，脂肪酸延伸，去饱和和氧化的基因表达变化。这篇综述汇集了代谢和分子研究，有助于解释肝基因转录的n-3（omega-3）多不饱和脂肪酸调控。最近的发现：膳食n-3多不饱和脂肪酸通过靶向三个主要的转录调节网络来调节肝基因表达：过氧化物酶体增殖物激活受体α，固醇调节元素结合蛋白-1和碳水化合物调节元素结合蛋白/ Max样因子X异二聚体。 22：6，n-3是组织中最主要的n-3多不饱和脂肪酸，是过氧化物酶体增殖物激活受体α的弱激活剂。但是，肝的22：6，n-3代谢会产生20：5，n-3，这是一种强大的过氧化物酶体增殖物激活的受体α激活剂。与过氧化物酶体增殖物激活的受体α相反，22：6，n-3是肝固醇调节元件结合蛋白-1中最有效的脂肪酸调节剂。 22：6，n-3抑制了固醇调节元件结合蛋白-1基因的表达，同时通过26S蛋白酶体和Erk1 / 2依赖性机制增强了核固醇调节元件结合蛋白1的降解。 n-3和n-6多不饱和脂肪酸均抑制碳水化合物调节元件结合蛋白和Max-like因子X核丰度，并干扰葡萄糖调节的肝代谢。摘要：这些研究揭示了独特的机制，通过这些机制，特定的多不饱和脂肪酸可控制过​​氧化物酶体增殖物激活的受体α，固醇调节元件结合蛋白-1和碳水化合物调节元件结合蛋白/ Max样因子X的功能。这样，特定的代谢和信号转导途径对这些转录因子及其相应的调节网络的脂肪酸调节起重要作用。

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