脂质代谢与肥胖的基因组科学。

Forum of Nutrition Pub Date : 2009-01-01 Epub Date: 2009-04-07 DOI:10.1159/000212736
Nobuyuki Takahashi, Tsuyoshi Goto, Shizuka Hirai, Taku Uemura, Teruo Kawada
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引用次数: 9

摘要

脂质代谢异常导致肥胖,导致代谢综合征。因此,改善这些异常对代谢综合征的治疗具有重要意义。特定配体激活的核受体在基因组水平上调节脂质代谢。脂质代谢相关酶的表达受各种核受体活性的影响而增加或减少。酶的表达调控是由靶基因启动子中对每个核受体的特异性应答元件介导的。许多食物因子作为激动剂或拮抗剂控制核受体的活性。在这里,我们提供了几个食物因子作为激动剂或拮抗剂的例子,这对于肥胖伴随脂质代谢异常的管理是有用的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Genome science of lipid metabolism and obesity.

Abnormalities in lipid metabolism cause obesity leading to metabolic syndrome. Thus, improvement of the abnormalities is significant for the treatment of metabolic syndrome. Nuclear receptors activated by specific ligands regulate lipid metabolism at the genomic level. The expression of lipid metabolism-related enzymes is increased or decreased by the activity of various nuclear receptors. The regulation of enzyme expression is mediated by specific response elements to each nuclear receptor in promoters of target genes. Many food factors acting as agonists or antagonists control the activities of nuclear receptors. Here, we provide several examples of food factors acting as agonists or antagonists, which are useful for the management of obesity accompanied by lipid metabolism abnormalities.

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