Genetic flaws could explain why some people develop type 2 diabetes and others do not, according to US researchers.
Scientists from leading universities across the US believe the answer lies in how pancreatic cells “read” genes which have previously been linked to diabetes.
“We have found that many of the subtle DNA spelling differences that increase risk of type 2 diabetes appears to disrupt a common regulatory grammar in islet cells,” said Dr Stephen Parker, an assistant professor of computational medicine and bioinformatics, and of human genetics, at the U-M Medical School, and one of four senior authors of the study.
Genetics have long been associated with the development of type 2 diabetes, but these findings do not negate the importance of eating a healthy diet and getting regular exercise in reducing the risk of type 2 diabetes.
Parker and colleagues discovered that a DNA-reading molecule called Regulatory Factor X (RFX) is significant in this process.
“RFX is probably unable to read the misspelled words, and this disruption of regulatory grammar plays a significant role in the genetic risk of type 2 diabetes,” Parker said.
The researchers examined DNA taken from islet samples of 112 people, none of whom had diabetes at the start of the study. Differences in the DNA sequences were noted, which helped the study team to track how RFX worked.
The function of the RFX is to bind to a stretch of DNA near the gene – but when genes linked to type 2 diabetes are present, that stretch of DNA can become disturbed, which affects the RFX binding process.
Changes to each DNA signature could affect RFX binding in different ways, either increasing risk of type 2 diabetes or by changing blood sugar regulation. But the common factor of this affected process was its effect on the area where RFX is believed to bind to insulin-producing cells.
“Genetic variants that increase T2D risk are predicted to disrupt RFX binding, providing a molecular mechanism to explain how the genome can influence the epigenomen, modulating gene expression and ultimately T2D risk,” said the authors.
The paper, which appears in the journal Proceedings of the National Academy of Sciences, was compiled by researchers from the National Institutes of Health, Jackson Laboratory for Genomic Medicine, University of North Carolina, the University of Southern California, as well as the University of Michigan.

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