多囊卵巢综合征肥胖分子机制的生物信息学分析。
Bioinformatics analysis of the molecular mechanism of obesity in polycystic ovary syndrome.
机构信息
Department of Endocrinology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, China.
Department of Endocrinology, The Affiliated Wujin Hospital of Jiangsu University, Changzhou, Jiangsu 213017, China.
出版信息
Aging (Albany NY). 2021 Apr 27;13(9):12631-12640. doi: 10.18632/aging.202938.
BACKGROUND
Obesity is an important part of polycystic ovary syndrome (PCOS) pathologies. The present study utilized the bioinformatics method to identify the molecular mechanism of obesity status in PCOS.
METHODS
Six transcriptome profiles of adipose tissue were obtained from online databases. The background correction and normalization were performed, and the DEGs were detected with the settings < 0.05. The GO, KEGG pathway enrichment, and PPI network analysis were performed with the detected DEGs.
RESULTS
A total of 37 DGEs were found between obesity PCOS and healthy controls, and 8 of them were tested significant in the third database. The expression patterns of the 8 detected DGEs were then measured in another two datasets based on lean/obesity PCOS patients and healthy controls. The gene CHRDL1 was found to be in linear regression with the BMI index in PCOS patients ( = 0.0358), but such a difference was not found in healthy controls ( = 0.2487). The expression of CHRDL1 was significantly higher in obesity PCOS cases than the BMI matched healthy controls ( = 0.0415). Further enrichment research demonstrated the CHRDL1 might function as an inhibitor of the BMP4 or IGF1 signalling.
CONCLUSION
In summary, the present study identified CHRDL1 as a candidate gene responsible for the obesity of PCOS patients.
背景
肥胖是多囊卵巢综合征（PCOS）病理的重要组成部分。本研究利用生物信息学方法来鉴定 PCOS 中肥胖状态的分子机制。
方法
从在线数据库中获取 6 个脂肪组织转录组谱。进行背景校正和归一化，并设置 < 0.05 检测差异表达基因（DEGs）。利用检测到的 DEGs 进行 GO、KEGG 通路富集和 PPI 网络分析。
结果
在肥胖 PCOS 和健康对照组之间共发现 37 个 DGEs，其中 8 个在第三个数据库中检测到显著差异。然后，根据瘦/肥胖 PCOS 患者和健康对照组，在另外两个数据集上测量了这 8 个检测到的 DGEs 的表达模式。发现 CHRDL1 基因在 PCOS 患者的 BMI 指数上呈线性回归（ = 0.0358），但在健康对照组中没有发现这种差异（ = 0.2487）。CHRDL1 在肥胖 PCOS 病例中的表达明显高于 BMI 匹配的健康对照组（ = 0.0415）。进一步的富集研究表明，CHRDL1 可能作为 BMP4 或 IGF1 信号的抑制剂发挥作用。
结论
总之，本研究鉴定出 CHRDL1 是导致 PCOS 患者肥胖的候选基因。
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