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首页> 外文期刊>Molecular and Cellular Biology >Activated Liver X Receptors Stimulate Adipocyte Differentiation through Induction of Peroxisome Proliferator-Activated Receptor γ Expression
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Activated Liver X Receptors Stimulate Adipocyte Differentiation through Induction of Peroxisome Proliferator-Activated Receptor γ Expression

机译：活化的肝X受体通过过氧化物酶体增殖物激活的受体γ表达的诱导来刺激脂肪细胞分化。

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Liver X receptors (LXRs) are nuclear hormone receptors that regulate cholesterol and fatty acid metabolism in liver tissue and in macrophages. Although LXR activation enhances lipogenesis, it is not well understood whether LXRs are involved in adipocyte differentiation. Here, we show that LXR activation stimulated the execution of adipogenesis, as determined by lipid droplet accumulation and adipocyte-specific gene expression in vivo and in vitro. In adipocytes, LXR activation with T0901317 primarily enhanced the expression of lipogenic genes such as the ADD1/SREBP1c and FAS genes and substantially increased the expression of the adipocyte-specific genes encoding PPARγ (peroxisome proliferator-activated receptor γ) and aP2. Administration of the LXR agonist T0901317 to lean mice promoted the expression of most lipogenic and adipogenic genes in fat and liver tissues. It is of interest that the PPARγ gene is a novel target gene of LXR, since the PPARγ promoter contains the conserved binding site of LXR and was transactivated by the expression of LXRα. Moreover, activated LXRα exhibited an increase of DNA binding to its target gene promoters, such as ADD1/SREBP1c and PPARγ, which appeared to be closely associated with hyperacetylation of histone H3 in the promoter regions of those genes. Furthermore, the suppression of LXRα by small interfering RNA attenuated adipocyte differentiation. Taken together, these results suggest that LXR plays a role in the execution of adipocyte differentiation by regulation of lipogenesis and adipocyte-specific gene expression.
机译：肝脏X受体（LXR）是核激素受体，可调节肝组织和巨噬细胞中的胆固醇和脂肪酸代谢。尽管LXR的激活增强了脂肪的生成，但还不清楚LXR是否参与脂肪细胞的分化。在这里，我们显示LXR激活刺激了脂肪形成的执行，这由体内和体外的脂质滴积累和脂肪细胞特异性基因表达确定。在脂肪细胞中，用T0901317进行的LXR激活主要增强了脂肪形成基因（如ADD1 / SREBP1c和FAS基因）的表达，并大大提高了编码PPARγ（过氧化物酶体增殖物激活的受体γ）和aP2的脂肪细胞特异性基因的表达。向瘦小鼠施用LXR激动剂T0901317可以促进脂肪和肝组织中大多数脂肪形成和脂肪形成基因的表达。有趣的是，PPARγ基因是LXR的新靶基因，因为PPARγ启动子包含LXR的保守结合位点，并通过LXRα的表达而被激活。而且，活化的LXRα显示出与其靶基因启动子如ADD1 / SREBP1c和PPARγ的DNA结合的增加，这似乎与那些基因的启动子区域中组蛋白H3的超乙酰化密切相关。此外，小干扰RNA抑制LXRα减弱了脂肪细胞的分化。综上所述，这些结果表明LXR通过调节脂肪生成和脂肪细胞特异性基因表达在脂肪细胞分化的执行中发挥作用。

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