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肥胖导致代谢综合征过程中异常产热素表达(UCP1)的遗传背景。

Genetic background of aberrant thermogenin expression (UCP1) in obesity leading to metabolic syndrome.

作者信息

Stosio Małgorzata, Witkowicz Agata, Kowalska Anna, Karabon Lidia

机构信息

Instytut Immunologii i Terapii Doświadczalnej PAN im. L. Hirszfelda we Wrocławiu.

Instytut Immunologii i Terapii Doświadczalnej PAN im. L. Hirszfelda we Wrocławiu; Insytut Genetyki Człowieka PAN w Poznaniu.

出版信息

Postepy Hig Med Dosw (Online). 2016 Dec 31;70(0):1389-1403. doi: 10.5604/17322693.1227677.

DOI:10.5604/17322693.1227677
PMID:28100847
Abstract

Cardiovascular and metabolic disturbances individually and interdependently lead to chronic pathological conditions observed in cardio-metabolic diseases (CMDs). In Europe, the morbidity and mortality caused by cardiovascular disease are the highest among all diseases. Therefore, it seems important to search for new and alternative therapies for obesity, which is the main cause of type 2 diabetes (T2D) and cardiovascular disease (CD). Great attention has been paid to the role of brown adipose tissue in fat burning and the possibility of transformation of the white adipose tissue to cells with brown adipose tissue function as a potential form of treatment of obesity. The best-characterized marker of brown adipose tissue is uncoupling protein 1 (UCP1), which has the ability to dissipate energy as heat in the process called non-shivering thermogenesis. Numerous studies have shown that altered expression of this protein can lead to disturbances in fat metabolism. One possible reason for the aberrant expression of UCP1 may be inherited variations in the gene encoding that protein. Therefore, several studies investigating the role of polymorphisms in the gene encoding UCP1 in susceptibility to obesity or metabolic syndrome have been performed. Here we summarize the results of studies describing the associations between the UCP1 gene polymorphisms A-3826G, A-1766G, Met229Leu and Ala64Thr and polymorphism Trp64Arg in the β3-AR gene, their correlations and their associations with the occurrence of metabolic syndrome.

摘要

心血管和代谢紊乱单独或相互依赖地导致在心脏代谢疾病(CMD)中观察到的慢性病理状况。在欧洲,心血管疾病导致的发病率和死亡率在所有疾病中是最高的。因此,寻找针对肥胖症的新的和替代疗法似乎很重要,肥胖症是2型糖尿病(T2D)和心血管疾病(CD)的主要原因。棕色脂肪组织在脂肪燃烧中的作用以及白色脂肪组织向具有棕色脂肪组织功能的细胞转化作为肥胖症潜在治疗形式的可能性受到了极大关注。棕色脂肪组织最具特征的标志物是解偶联蛋白1(UCP1),它能够在称为非颤抖性产热的过程中将能量以热量形式消散。大量研究表明,这种蛋白质表达的改变会导致脂肪代谢紊乱。UCP1异常表达的一个可能原因可能是编码该蛋白质的基因中的遗传变异。因此,已经进行了几项研究来调查UCP1基因多态性在肥胖症或代谢综合征易感性中的作用。在这里,我们总结了描述UCP1基因多态性A - 3826G、A - 1766G、Met229Leu和Ala64Thr以及β3 - AR基因中的多态性Trp64Arg之间的关联、它们的相关性以及它们与代谢综合征发生之间关联的研究结果。

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