Bioinformatics analysis of the molecular mechanism of obesity in polycystic ovary syndrome

Aging (Albany NY). 2021 Apr 27;13(9):12631-12640. doi: 10.18632/aging.202938. Epub 2021 Apr 27.

Abstract

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.

Keywords: CHRDL1; PCOS; bioinformatics; obesity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Body Mass Index
  • Bone Morphogenetic Protein 4 / genetics
  • Eye Proteins / genetics
  • Eye Proteins / metabolism
  • Female
  • Humans
  • Insulin-Like Growth Factor I / genetics
  • Insulin-Like Growth Factor I / metabolism
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism
  • Obesity / genetics*
  • Obesity / metabolism*
  • Polycystic Ovary Syndrome / genetics*
  • Polycystic Ovary Syndrome / metabolism*
  • Signal Transduction / genetics
  • Signal Transduction / physiology

Substances

  • BMP4 protein, human
  • Bone Morphogenetic Protein 4
  • CHRDL1 protein, human
  • Eye Proteins
  • IGF1 protein, human
  • Nerve Tissue Proteins
  • Insulin-Like Growth Factor I