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首页> 外文期刊>Cell metabolism >Hepatic Deficiency in Transcriptional Cofactor TBL1 Promotes Liver Steatosis and Hypertriglyceridemia.
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Hepatic Deficiency in Transcriptional Cofactor TBL1 Promotes Liver Steatosis and Hypertriglyceridemia.

机译：转录辅助因子TBL1的肝功能不足会促进肝脂肪变性和高甘油三酯血症。

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The aberrant accumulation of lipids in the liver ("fatty liver") is tightly associated with several components of the metabolic syndrome, including type 2 diabetes, coronary heart disease, and atherosclerosis. Here we show that the impaired hepatic expression of transcriptional cofactor transducin beta-like (TBL) 1 represents a common feature of mono- and multigenic fatty liver mouse models. Indeed, the liver-specific ablation of TBL1 gene expression in healthy mice promoted hypertriglyceridemia and hepatic steatosis under both normal and high-fat dietary conditions. TBL1 deficiency resulted in inhibition of fatty acid oxidation due to impaired functional cooperation with its heterodimerization partner TBL-related (TBLR) 1 and the nuclear receptor peroxisome proliferator-activated receptor (PPAR) alpha. As TBL1 expression levels were found to also inversely correlate with liver fat content in human patients, the lack of hepatic TBL1/TBLR1 cofactor activity may represent a molecular rationale for hepatic steatosis in subjects with obesity and the metabolic syndrome.
机译：脂质在肝脏（“脂肪肝”）中的异常积累与代谢综合征的某些成分紧密相关，包括2型糖尿病，冠心病和动脉粥样硬化。在这里，我们显示转录辅因子转导蛋白β样（TBL）1的肝表达受损代表单基因和多基因脂肪肝小鼠模型的共同特征。实际上，在正常和高脂饮食条件下，健康小鼠中TBL1基因表达的肝脏特异性消融促进了高甘油三酯血症和肝脂肪变性。 TBL1缺乏症导致脂肪酸氧化受到抑制，这是由于与其异二聚体伴侣TBL相关（TBLR）1和核受体过氧化物酶体增殖物激活受体（PPAR）α的功能协作受损。由于发现人类患者中TBL1表达水平也与肝脂肪含量呈负相关，因此，肝TBL1 / TBLR1辅助因子活性的缺乏可能代表了肥胖症和代谢综合征患者肝脂肪变性的分子原理。

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