Open Access

Microarray analysis of differentially expressed genes and their functions in omental visceral adipose tissues of pregnant women with vs. without gestational diabetes mellitus

  • Authors:
    • Yuan Qian
    • Hao Sun
    • Hongli Xiao
    • Meirun Ma
    • Xue Xiao
    • Qinzai Qu
  • View Affiliations

  • Published online on: March 22, 2017     https://doi.org/10.3892/br.2017.878
  • Pages: 503-512
  • Copyright: © Qian et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Increasing evidence has shown that insulin resistance in omental visceral adipose tissue (OVAT) is a characteristic of gestational diabetes mellitus (GDM). The present study aimed to identify differentially expressed genes (DEGs) and their associated functions and pathways involved in the pathogenesis of GDM by comparing the expression profiles of OVATs obtained from pregnant Chinese women with and without GDM during caesarian section. A total of 935 DEGs were identified, including 450 downregulated and 485 upregulated genes. In the gene ontology category cellular components, the DEGs were predominantly associated with functions of the extracellular region, while receptor binding was predominant in the molecular function category and biological process terms included antigen processing and presentation, extracellular matrix organization, positive regulation of cell‑substrate adhesion, response to nutrients and response to dietary excess. Functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were performed and a functional interaction network was constructed. Functions of downregulated genes included antigen processing and presentation as well as cell adhesion molecules, while those of upregulated genes included transforming growth factor (TGF)‑β‑signaling, focal adhesion, phosphoinositide‑3 kinase‑Akt‑signaling, P53 signaling, extracellular matrix‑receptor interaction and regulation of actin cytoskeleton pathway. The five main pathways associated with GDM were antigen processing and presentation, cell adhesion molecules, Type 1 diabetes mellitus, natural killer cell‑mediated cytotoxicity and TGF‑β signaling. These pathways were included in the KEGG pathway categories of ‘signaling molecules and interaction’, ‘immune system’ and ‘inflammatory response’, suggesting that these processes are involved in GDM. The results of the present study enhanced the present understanding of the mechanisms associated with insulin resistance in OVATs of GDM.
View Figures
View References

Related Articles

Journal Cover

May-2017
Volume 6 Issue 5

Print ISSN: 2049-9434
Online ISSN:2049-9442

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Qian Y, Sun H, Xiao H, Ma M, Xiao X and Qu Q: Microarray analysis of differentially expressed genes and their functions in omental visceral adipose tissues of pregnant women with vs. without gestational diabetes mellitus. Biomed Rep 6: 503-512, 2017
APA
Qian, Y., Sun, H., Xiao, H., Ma, M., Xiao, X., & Qu, Q. (2017). Microarray analysis of differentially expressed genes and their functions in omental visceral adipose tissues of pregnant women with vs. without gestational diabetes mellitus. Biomedical Reports, 6, 503-512. https://doi.org/10.3892/br.2017.878
MLA
Qian, Y., Sun, H., Xiao, H., Ma, M., Xiao, X., Qu, Q."Microarray analysis of differentially expressed genes and their functions in omental visceral adipose tissues of pregnant women with vs. without gestational diabetes mellitus". Biomedical Reports 6.5 (2017): 503-512.
Chicago
Qian, Y., Sun, H., Xiao, H., Ma, M., Xiao, X., Qu, Q."Microarray analysis of differentially expressed genes and their functions in omental visceral adipose tissues of pregnant women with vs. without gestational diabetes mellitus". Biomedical Reports 6, no. 5 (2017): 503-512. https://doi.org/10.3892/br.2017.878