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肥胖管理的新希望:硼通过Wnt/β-连环蛋白途径抑制祖细胞中的脂肪生成。

A new hope for obesity management: Boron inhibits adipogenesis in progenitor cells through the Wnt/β-catenin pathway.

作者信息

Doğan Ayşegül, Demirci Selami, Apdik Hüseyin, Bayrak Omer Faruk, Gulluoglu Sukru, Tuysuz Emre Can, Gusev Oleg, Rizvanov Albert A, Nikerel Emrah, Şahin Fikrettin

机构信息

Department of Genetics and Bioengineering, Faculty of Engineering, Yeditepe University, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755 Atasehir, Istanbul, Turkey; National Cancer Instıtute, CDBL, NIH, Frederıck, MD.

Department of Genetics and Bioengineering, Faculty of Engineering, Yeditepe University, Kayisdagi Cad. 26 Agustos Yerlesimi, 34755 Atasehir, Istanbul, Turkey; National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD.

出版信息

Metabolism. 2017 Apr;69:130-142. doi: 10.1016/j.metabol.2017.01.021. Epub 2017 Jan 19.

DOI:10.1016/j.metabol.2017.01.021
PMID:28285642
Abstract

Obesity is a worldwide medical problem resulting in serious morbidity and mortality involving differentiation of pre-adipocytes into mature adipocytes (adipogenesis). Boron treatment has been reported to be associated with weight reduction in experimental animals; however, its effects on pre-adipocyte differentiation and anti-adipogenic molecular mechanisms are unknown. In this study, we demonstrate the inhibitory activities of boric acid (BA) and sodium pentaborate pentahydrate (NaB) on adipogenesis using common cellular models. Boron treatment repressed the expression of adipogenesis-related genes and proteins, including CCAAT-enhancer-binding protein α and peroxisome proliferator-activated receptor γ, by regulating critical growth factors and the β-catenin, AKT, and extracellular signal-regulated kinase signaling pathways. In addition, although boron treatment did not induce apoptosis in pre-adipocytes, it depressed mitotic clonal expansion by regulation of cell cycle genes. Overall, these data offer promising insights into the prevention/treatment of obesity and associated diseases.

摘要

肥胖是一个全球性的医学问题,会导致严重的发病率和死亡率,涉及前脂肪细胞分化为成熟脂肪细胞(脂肪生成)。据报道,硼处理与实验动物体重减轻有关;然而,其对前脂肪细胞分化和抗脂肪生成分子机制的影响尚不清楚。在本研究中,我们使用常见的细胞模型证明了硼酸(BA)和五水硼酸钠(NaB)对脂肪生成的抑制活性。硼处理通过调节关键生长因子以及β-连环蛋白、AKT和细胞外信号调节激酶信号通路,抑制了脂肪生成相关基因和蛋白质的表达,包括CCAAT增强子结合蛋白α和过氧化物酶体增殖物激活受体γ。此外,虽然硼处理未诱导前脂肪细胞凋亡,但通过调节细胞周期基因抑制了有丝分裂克隆扩增。总体而言,这些数据为肥胖及相关疾病的预防/治疗提供了有前景的见解。

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