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Biomed Rep. 2017 May;6(5):503-512. doi: 10.3892/br.2017.878. Epub 2017 Mar 22.

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

Yuan Qian, Hao Sun, Hongli Xiao, Meirun Ma, Xue Xiao, Qinzai Qu

Affiliations

  1. Pre-natal Diagnosis Laboratory, Department of Obstetrics and Gynaecology, The First Affiliated Hospital of Kunming Medical College, Kunming, Yunnan 650032, P.R. China.
  2. Department of Human Genetics, Genetics Laboratory, The Institute of Medical Biology, Chinese Academy of Medical Science, Kunming, Yunnan 650032, P.R. China.

PMID: 28529732 PMCID: PMC5431681 DOI: 10.3892/br.2017.878

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.

Keywords: differentially expressed gene; expression profile; functional enrichment analysis; gestational diabetes mellitus; insulin resistance; interaction network

References

  1. J Endocrinol. 2013 Jul 01;218(2):165-78 - PubMed
  2. Nat Rev Mol Cell Biol. 2008 May;9(5):367-77 - PubMed
  3. Acta Diabetol. 2015 Feb;52(1):153-60 - PubMed
  4. Diabetes Metab Res Rev. 2001 Nov-Dec;17(6):422-8 - PubMed
  5. Placenta. 2006 Aug;27(8):794-8 - PubMed
  6. Diabetologia. 2007 Oct;50(10 ):2036-41 - PubMed
  7. Nat Rev Genet. 2006 Jan;7(1):55-65 - PubMed
  8. Biochim Biophys Acta. 2012 Jun;1822(6):1030-7 - PubMed
  9. BMC Clin Pathol. 2013 May 24;13:16 - PubMed
  10. Chem Biol Drug Des. 2015 Nov;86(5):1064-71 - PubMed
  11. Ann N Y Acad Sci. 2012 Oct;1271:82-7 - PubMed
  12. Hepatology. 2014 Feb;59(2):483-95 - PubMed
  13. BMC Endocr Disord. 2016 Sep 29;16(1):52 - PubMed
  14. J Proteome Res. 2016 Feb 5;15(2):628-37 - PubMed
  15. J Biol Chem. 2000 Dec 8;275(49):38371-7 - PubMed
  16. Biochim Biophys Acta. 2014 Mar;1842(3):446-62 - PubMed
  17. BMC Cell Biol. 2008 Sep 04;9:48 - PubMed
  18. Eur J Immunol. 2008 Nov;38(11):2961-3 - PubMed
  19. Cancer Res. 2015 Jan 1;75(1):40-50 - PubMed
  20. J Hepatol. 2010 Jun;52(6):913-20 - PubMed
  21. Rev Assoc Med Bras (1992). 2015 Jan-Feb;61(1):72-80 - PubMed
  22. Am J Reprod Immunol. 2006 Aug;56(2):124-34 - PubMed
  23. Obes Rev. 2010 Jan;11(1):11-8 - PubMed
  24. Trends Genet. 2006 Feb;22(2):101-9 - PubMed
  25. Clin Epigenetics. 2015 Aug 05;7:79 - PubMed
  26. OMICS. 2007 Spring;11(1):25-40 - PubMed
  27. BMC Med Genomics. 2014 May 23;7:28 - PubMed
  28. Int J Cancer. 2015 Oct 1;137(7):1621-9 - PubMed
  29. Mol Cell Endocrinol. 2012 Nov 5;363(1-2):10-9 - PubMed
  30. Science. 2003 Dec 5;302(5651):1710-1 - PubMed
  31. Mol Med Rep. 2015 Mar;11(3):1963-7 - PubMed
  32. N Engl J Med. 1999 Dec 2;341(23):1749-56 - PubMed
  33. Cancer Chemother Pharmacol. 2015 Jun;75(6):1207-15 - PubMed
  34. J Clin Invest. 2011 Jun;121(6):2111-7 - PubMed
  35. Mol Biol Cell. 2012 Oct;23 (19):3882-98 - PubMed
  36. Genet Epidemiol. 2014 Dec;38(8):661-70 - PubMed
  37. Anticancer Res. 2014 Oct;34(10):5599-607 - PubMed
  38. Pharmacogenomics J. 2015 Dec;15(6):538-48 - PubMed
  39. Endokrynol Pol. 2014;65(2):134-42 - PubMed
  40. J Clin Invest. 2006 Jul;116(7):1756-60 - PubMed
  41. Cancer Med. 2014 Aug;3(4):835-44 - PubMed
  42. Cancers (Basel). 2015 Jan 07;7(1):96-111 - PubMed
  43. Diabet Med. 2011 Feb;28(2):237-46 - PubMed
  44. Lancet Diabetes Endocrinol. 2014 Jun;2(6):488-99 - PubMed

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