Display options
Share it on

Indian J Endocrinol Metab. 2016 Jul-Aug;20(4):523-30. doi: 10.4103/2230-8210.183474.

Gut Microbiota in Type 2 Diabetes Individuals and Correlation with Monocyte Chemoattractant Protein1 and Interferon Gamma from Patients Attending a Tertiary Care Centre in Chennai, India.

Indian journal of endocrinology and metabolism

Premalatha Pushpanathan, Padma Srikanth, Krishna G Seshadri, Sribal Selvarajan, Ravi Shankar Pitani, Thomas David Kumar, R Janarthanan

Affiliations

  1. Department of Microbiology, Sri Ramachandra Medical College and Research Institute, Sri Ramachandra University, Porur, Chennai, Tamil Nadu, India.
  2. Department of Endocrinology, Sri Ramachandra Medical College and Research Institute, Sri Ramachandra University, Porur, Chennai, Tamil Nadu, India.
  3. Department of Community Medicine, Sri Ramachandra Medical College and Research Institute, Sri Ramachandra University, Porur, Chennai, Tamil Nadu, India.
  4. Shrimpex Biotech Services Private Limited, Sholinganallur, Chennai, Tamil Nadu, India.

PMID: 27366720 PMCID: PMC4911843 DOI: 10.4103/2230-8210.183474

Abstract

BACKGROUND: Type 2 diabetes mellitus (T2DM) and obesity are associated with changes in gut microbiota and characterized by chronic low-grade inflammation. Monocyte chemoattractant protein-1 (MCP-1) and interferon gamma (IFNγ) are proinflammatory cytokines which play an important role in the development of T2DM. We undertook this study to analyze the gut microbiota of T2DM and nondiabetic subjects and to determine the profile of MCP 1 and IFNγ in the same subjects attending a tertiary care center in Chennai, Tamil Nadu, India.

METHODS: The study included 30 subjects with clinical details. Stool and blood samples were collected from all the subjects. DNA was extracted from fecal samples and polymerase chain reaction was done using fusion primers. Metagenomic analysis was performed using ion torrent sequencing. The reads obtained were in FASTA format and reported as operational taxonomic units. Human MCP 1 and IFNγ enzyme linked immunosorbent assay (ELISA) were performed for 23 serum samples.

RESULTS: The study consisted of 30 subjects; 17 were T2DM and 13 were nondiabetics. The gut microbiota among T2DM consisted predominantly of Gram negative bacteria; Escherichia and Prevotella, when compared with the nondiabetic group with predominantly Gram positive organisms suchas Faecalibacterium, Eubacterium, and Bifidobacterium. The mean MCP-1 values in the diabetic group were 232.8 pg/ml and in the nondiabetic group 170.84 pg/ml. IFNγ (mean 385.5 pg/ml) was raised in glycated hemoglobin (HbA1c) group of 6.5-7.5% which was statistically significant. Association of Escherichia with T2DM and association of Bifidobacteria in the nondiabetics were also statistically significant.

CONCLUSION: Escherichia counts were elevated in T2DM with HbA1c of 6.5-8.5% which was statistically significant suggesting that lipopolysaccharides present in the cell wall of Gram-negative bacteria may be responsible for low-grade inflammation as evidenced by elevated MCP-1 and IFNγ levels in T2DM with the same HbA1c levels.

Keywords: Gut microbiota; glycated hemoglobin; interferon gamma; metagenomic sequencing; monocyte chemoattractant protein-1; nondiabetes; type 2 diabetes mellitus

References

  1. Nature. 2015 Mar 5;519(7541):92-6 - PubMed
  2. J Trauma. 2006 Sep;61(3):650-7 - PubMed
  3. PLoS One. 2010 Feb 05;5(2):e9085 - PubMed
  4. PLoS One. 2015 Nov 12;10(11):e0142352 - PubMed
  5. Nature. 2014 Oct 9;514(7521):181-6 - PubMed
  6. Proc Natl Acad Sci U S A. 2005 Aug 2;102(31):11070-5 - PubMed
  7. Rev Diabet Stud. 2012 Spring;9(1):6-22 - PubMed
  8. Am J Med. 2002 Feb 15;112(3):204-11 - PubMed
  9. Nature. 2012 May 09;486(7402):222-7 - PubMed
  10. Int J Endocrinol. 2013;2013:976810 - PubMed
  11. Dig Dis Sci. 2004 Apr;49(4):579-89 - PubMed
  12. Diabetes Care. 2010 Oct;33(10):2277-84 - PubMed
  13. Cell. 2006 Feb 24;124(4):837-48 - PubMed
  14. Diabetologia. 2007 Nov;50(11):2374-83 - PubMed
  15. Clin Infect Dis. 2005 Feb 15;40(4):628-31 - PubMed
  16. Indian J Endocrinol Metab. 2014 Jul;18(4):505-10 - PubMed
  17. J Biol Chem. 2010 Dec 10;285(50):38751-5 - PubMed
  18. Diabetes. 2007 Jul;56(7):1761-72 - PubMed
  19. Trends Biotechnol. 2015 Sep;33(9):496-503 - PubMed
  20. Nature. 2013 Jun 6;498(7452):99-103 - PubMed

Publication Types