Researchers said 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.
