Low-protein diet fed to crossbred sows during pregnancy and lactation enhances myostatin gene expression through epigenetic regulation in skeletal muscle of weaning piglets

在怀孕和哺乳期间给杂交母猪饲喂低蛋白饮食可通过表观遗传调控增强断奶仔猪骨骼肌中的肌生长抑制素基因表达

阅读:5
作者:Yimin Jia, Guichao Gao, Haogang Song, Demin Cai, Xiaojing Yang, Ruqian Zhao

Conclusion

These results indicate that MSTN mediates maternal LP diet-induced growth retardation, through epigenetic regulation involving FoxO3 and GR binding to its promoter.

Methods

Sows were fed either a standard-protein (SP, 15 and 18 % crude protein) or a low-protein (LP, 50 % protein level of SP) diet throughout pregnancy and lactation. Longissimus dorsi muscle was sampled from male piglets at 28 days of age. The mRNA was determined by RT-PCR, and protein was measured by Western blot. Chromatin immunoprecipitation assay was used to determine the binding of transcription factors and histone H3 modifications on the MSTN gene promoter.

Purpose

This study was aimed to investigate the effects of a maternal low-protein diet on transcriptional regulation of the myostatin (MSTN) gene in skeletal muscle of weaning piglets.

Results

The maternal LP diet significantly decreased body weight and average daily gain (P < 0.05), which was associated with significantly lower plasma concentration of urea nitrogen and total protein (P < 0.05), as well as decreased muscle RNA content (P < 0.05). MSTN mRNA (P < 0.05) was significantly increased, together with enhanced (P < 0.05) mRNA and protein expression of forkhead box class O family member protein 3 (FoxO3), and a tendency of an increase (P = 0.10) in glucocorticoid receptor (GR) mRNA in the muscle of LP piglets. Furthermore, the binding of both FoxO3 and GR to the MSTN gene promoter was significantly higher (P < 0.05) in muscle of LP piglets, together with significantly enriched (P < 0.05) gene activation markers, H3K9Ac and H3K4me3.

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。