Open AccessBioinformatics analysis of the molecular mechanism of obesity in polycystic ovary syndrome
Author(s) -
Jiaojiao Zhou,
Xiaolin Huang,
Bingshuang Xue,
Yuhe Wei,
Hua Fang
Publication year - 2021
Publication title -
aging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.473
H-Index - 90
ISSN - 1945-4589
DOI - 10.18632/aging.202938
Subject(s) - polycystic ovary , mechanism (biology) , bioinformatics , biology , medicine , computational biology , obesity , endocrinology , insulin resistance , philosophy , epistemology
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 p < 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 ( p = 0.0358), but such a difference was not found in healthy controls ( p = 0.2487). The expression of CHRDL1 was significantly higher in obesity PCOS cases than the BMI matched healthy controls ( p = 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.