WASHINGTON (Reuters) - Researchers said on Sunday they had homed in on five areas of DNA that could account for 70 percent of the genetic risk for type-2 diabetes.
They identified four different areas of genetic variation that conferred a significant risk of developing diabetes and confirmed that a fifth area, a gene called TCF7L2 suspected in diabetes, is associated with the disease.
Writing in the journal Nature, the international team of researchers said their findings would help other scientists find causes and possible treatments for diabetes. They also said it showed it was useful to scan people’s entire genomes to look for disease-causing genes.
“Our new findings mean that we can create a good genetic test to predict people’s risk of developing this type of diabetes,” said Philippe Froguel of Imperial College London, who worked on the study.
Type-2 or adult onset diabetes is becoming more and more common around the world and is even being found now in children. It is associated with a rich diet and a lack of exercise.
“The rapidly increasing prevalence of type 2 diabetes mellitus is thought to be due to environmental factors, such as increased availability of food and decreased opportunity and motivation for physical activity, acting on genetically susceptible individuals,” the researchers wrote.
Constantin Polychronakos of McGill University in Montreal, Quebec, and colleagues tested nearly 7,000 volunteers — most with diabetes and many with a known family history of the disease.
They used new gene chip technology that allowed them to quickly screen for many of the tiny differences in the complex genetic code of DNA.
They found four new areas that appear involved in insulin secretion and pancreatic development. One gene encodes a protein that helps move zinc ions around and is found solely in the beta cells, the pancreatic cells that make and release insulin.
Many of the diabetes-linked variations seem to be the “older” version of the DNA sequence, suggesting that human beings evolved to be susceptible to diabetes. This would support the theory that biological traits that helped human beings survive famines have become disease-causing in times of plenty, they said.