Evaluation for CpG island methylation of FASN and SREBP promoter in Mongolian gerbil NAFLD model

蒙古沙鼠NAFLD模型中FASN和SREBP启动子CpG岛甲基化的评估

阅读:2
作者:Jiusheng Wu,Yuehuan Liu

Abstract

Introduction: Methylation of the CpG island in the promoter and its nearby area is one of the most important ways to inhibit gene expression. The aim of this study was to examine the potential relationship between CpG island methylation for fatty acid synthase (FASN) and sterol regulatory element-binding protein 1 (SREBP-1). Material and methods: Ten newborn gerbil pups formed the NB group, 10 adult gerbils with a normal diet formed the control group, 10 adult gerbils with a high-fat diet formed the nonalcoholic fatty liver disease (NAFLD) group, and 10 8-month-old gerbils formed the aged group. Blood and liver samples were collected for serum lipid detection and histopathology. A pyrosequencing technique was employed to determine the methylation rate. Then, the transcription and expression levels for FASN and SREBP-1 were verified. Results: Serum cholesterol and triglyceride were significantly increased in NAFLD and aged groups (vs. control, p < 0.05). The gerbils in NAFLD and aged groups also showed obvious hepatic steatosis confirmed by histological examination. The control group had the highest methylation rates for FASN and SREBP-1, which were reduced in NAFLD and aged groups. Except for the NB group, both the transcription and expression levels of SREBP-1 and FASN genes were in the following order: control group > aged group > NAFLD group. Genes of SREBP and FASN showed a trend of hypomethylation in the NAFLD gerbil model. Conclusions: Expression of the SREBP gene tended to decrease, while expression of the FASN gene tended to increase with age and disease development. FASN and SREBP-1 methylation might be a new method to evaluate an NAFLD animal model and an available target for genetic marker screening.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。