Jumping Gene Staves Off Type 2 Diabetes

New research 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……

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.

Stephan Scherneck, first author of the study was quoted as saying, “Our data suggest that the protein product of the risk gene in obese individuals enhances the storage of fat in fat cells…. 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.”