Researchers have discovered that so-called “junk DNA” could provide further understanding of how diabetes develops.
According to an international team led by Imperial College London, “junk DNA” is the name given to regions of non-coding DNA.
These chunks of non-coding DNA were not previously thought to have a function in humans, but new findings suggest they play an important role in the pancreas, the organ central to the development of diabetes.
The study results show specific non-protein coding regions control cells which produce the pancreatic cells needed to regulate blood sugar levels.
Professor Jorge Ferrer, who led the study, said: “There’s only a tiny proportion of the genome that codes for proteins. The rest of it was largely uncharted until a few years ago.
“But this non-coding DNA is now known to harbour many functional elements which regulate other genes.”
Ferrer and colleagues found there were long regions of junk DNA within pancreatic cells which were copied to ribonucleic acid (RNA). RNA strands typically carry the instructions for making proteins and can make DNA change shape.
One junk regio, known as PLUTO, was found next to a controlling gene called PDX1.
The role of PLUTO is to encourage beta cells to make insulin, and when the researchers realised the presence of PLUTO changed the way DNA around it folded, this suggested that advancing the gene’s activity would affect the beta cells.
“We know that these transcription factors are actually very important for human diabetes,” said Ferrer. “PDX1 is essential to countering the body’s growing resistance to insulin, so these genes are really important in terms of human diabetes – both inherited and acquired.”
PDX1 and PLUTO were both found to be less active in samples of tissue taken from people with type 2 diabetes, which the researchers say proves that PLUTO and other non-coding regions play an important part in keeping cells healthy.
Ferrer said: “These long non-coding RNAs are a new class of genes whose function we can now try to unravel. They could potentially be relevant to the mechanisms underlying diabetes.”
The study results have been published in the journal Cell Metabolism.

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