(Ivanhoe Newswire) -- Research led by the German Institute of Human
Nutrition has identified a genomic fragment, called a transposon, or "jumping
gene," that diminishes the activity of the diabetes risk gene in both mice and
humans.
Transposons are sequences of DNA that can move around to different positions
within the genome of a single cell, hence their nickname "jumping genes."
Researchers studied the genomes of mouse strains that were obese but had no
elevated blood glucose levels and were less susceptible to diabetes. They
compared these mice to other strains, which exhibited a severe malfunction of
fat and glucose metabolism as they continued to gain weight, causing them to
rapidly develop type 2 diabetes.
Researchers found that the difference between the two mouse strains lies in a
small fragment of genetic information, the "jumping gene." This genetic fragment
is of viral origin and is localized in a non-coding segment of the risk gene for
diabetes, whose effect it diminishes. Without this genetic fragment, the risk
gene is fully active and, in combination with obesity, leads to type 2 diabetes
in mice. A similar risk gene is also active in the fat tissues of overweight
people suffering from diabetes -- more so than in healthy people.
"Our data suggest that the protein product of the risk gene in obese individuals
enhances the storage of fat in fat cells," Stephan Scherneck, first author of
the study was quoted as saying. "As a result, excessive fat accumulates in the
liver and this in turn contributes to the development of diabetes."
"We have therefore discovered a new diabetes gene of similar importance in mice
and humans," says Hans-Georg Joost, head of the study and scientific director of
German Institute of Human Nutrition, "as well as a mechanism that has not been
described before in connection with the heredity of diabetes and obesity."
Joost continued, "This transposon is quite active and almost completely "turns
off" the Zfp69 [diabetes risk] gene. We have found indications that it is also
active in other mouse genes. Since the human genome is full of such fragments,
it is quite possible that they play a greater role than previously assumed."
According to the World Health Organization (WHO), approximately 1.6 billion
people worldwide are overweight. The number of people with type 2 diabetes has
increased accordingly to 230 million.
SOURCE: PLoS Genetics, July 3, 2009
