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Novel epigenetic markers for type 2 diabetes risk detected in human liver
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European researchers have identified epigenetic markers associated with type 2 diabetes risk in the tissue of the human liver, according to research presented at the 50th European Association for the Study of Diabetes Annual Meeting.
Through DNA methylation information, new pathways relevant to the pathophysiology of type 2 diabetes and novel targets for prevention and treatment of the chronic disease can be identified, according to the investigators.
Stéphane Cauchi, PhD, of the National Center for Scientific Research, Lille Pasteur Institute, France, and the European Genomic Institute for Diabetes, and colleagues analyzed genome-wide methylation patterns in the liver tissue in 96 patients with type 2 diabetes and 96 matched normoglycemic controls.
The scientists used Infinium Human Methylation 450 BeadChips (Illumina) for their analyses. They applied a beta-mixture quantile normalization method for correcting probe design bias.
In a subset of 24 patients with type 2 diabetes and 24 matched normoglycemic controls, genome-wide expression profiles were also assessed using HumanHT-12 v4 Expression BeadChips (Illumina).
The researchers identified 158 sites that were differentially methylated between patients with type 2 diabetes and controls, after Bonferroni correction for multiple comparisons (P<1.5 x 10-7).
When considered together, the sites tended to be hypo-methylated in patients with type 2 diabetes compared with normoglycemic controls (P=1 x 10-7).
Two of the cytosine methylation marks were located near functionally relevant candidate genes that were differentially expressed with type 2 diabetes vs. controls (P<4.2 x 10-4).
The scientists observed direct correlations between methylation levels and gene expressions (P<1 x 10-3). Associations were also detected with insulin resistance (P<3 x 10-3) and steatosis (P<3 x 10-5) were detected.
For more information:
Cauchi S. Abstract #233. Presented at: 50th EASD Annual Meeting; Sept. 16-19, 2014; Vienna.
Disclosure: The work was supported by the Société Francophone du Diabète.