Kbtbd11 gene expression in adipose tissue increases in response to feeding and affects adipocyte differentiation
Kbtbd11 gene expression in adipose tissue increases in response to feeding and affects adipocyte differentiation
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DOI：
10.1111/jdi.12995
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发表时间：
2019-07-01
影响因子：
3.2
通讯作者：
Iwamoto, Sadahiko
中科院分区：
文献类型：
--
作者：
Watanabe, Kazuhisa;Yoshida, Ken;Iwamoto, Sadahiko
目的/引言假定的肿瘤抑制基因KBTBD 11可能在肿瘤发生中起作用，并且与结直肠癌细胞的细胞凋亡和增殖相关。然而，Kbtbd 11在脂肪形成过程中的功能尚不清楚。本研究的目的是研究Kbtbd 11在3 T3-L1前脂肪细胞分化中的作用。材料和方法对于禁食-再喂养方案，使小鼠禁食24 h，然后进食食物12 h。腺病毒感染法检测Kbtbd 11对3 T3-L1细胞的作用，油红O染色法和实时荧光定量PCR法检测Kbtbd 11对3 T3-L1细胞的作用。结果与禁食状态相比，再进食状态下白色脂肪组织中Kbtbd 11信使核糖核酸（mRNA）的表达量显著增加。与普通饲料喂养的小鼠相比，饮食诱导的肥胖小鼠附睾白色脂肪组织中Kbtbd 11 mRNA水平显著增加。此外，Kbtbd 11 mRNA的表达在3 T3-L1细胞中以分化依赖的方式增加。通过腺病毒载体的感染，Kbtbd 11 mRNA的敲低显着抑制甘油三酯的积累和脂肪细胞分化的3 T3-L1细胞。相反，Kbtbd 11的过表达促进了3 T3-L1脂肪细胞的分化。结论Kbtbd 11基因在肥胖脂肪组织中表达增强，可能参与营养调节。此外，Kbtbd 11似乎是3 T3-L1细胞中脂肪细胞分化所必需的。总的来说，这些结果显示了Kbtbd 11的表达与脂肪积累之间的新联系，并表明Kbtbd 11是肥胖症的新治疗靶点。
Aims/Introduction The putative tumor suppressor gene, KBTBD11, might play a role in tumorigenesis, and is associated with cellular apoptosis and proliferation in colorectal cancer cells. However, the function of Kbtbd11 during adipogenesis is unknown. The aim of the present study was to investigate the role of Kbtbd11 in the differentiation of 3T3-L1 preadipocytes. Materials and Methods For the fasting-refeeding protocol, mice were subjected to fasting for 24 h, followed by a chow diet for 12 h. Adenovirus infection methods were used to examine the effect of Kbtbd11, and 3T3-L1 cells were analyzed with Oil Red O staining and real-time polymerase chain reaction. Results The white adipose tissue expression of Kbtbd11 messenger ribonucleic acid (mRNA) was significantly higher in the re-fed state than in the fasted state. Kbtbd11 mRNA levels were markedly increased in epididymal white adipose tissue of diet-induced obesity mice compared with those in the mice fed a chow diet. In addition, Kbtbd11 mRNA expression was increased in a differentiation-dependent manner in 3T3-L1 cells. Knockdown of Kbtbd11 mRNA through the infection with adenoviral vectors remarkably inhibited triglyceride accumulation and adipocyte differentiation in 3T3-L1 cells. In contrast, the overexpression of Kbtbd11 promoted the differentiation of 3T3-L1 adipocytes. Conclusions The present findings show that Kbtbd11 expression might be involved in nutritional regulation and is increased in obese adipose tissue. In addition, Kbtbd11 appears to be required for the differentiation of adipocytes in 3T3-L1 cells. Collectively, these results show a novel link between the expression of Kbtbd11 and fat accumulation, and suggest that Kbtbd11 is a new therapeutic target for obesity.