Scientists at the German Institute of Human Nutrition have announced the identification of a new gene that is associated with diabetes, and of a mechanism that makes obese mice less susceptible to diabetes.
The researchers say that a genomic fragment that occurs naturally in some mouse strains diminishes the activity of the risk gene Zfp69.
They have also found that the corresponding human gene (ZNF642) is especially active in overweight individuals with diabetes.
They revealed that some of the obese mice had no strikingly elevated blood glucose levels, and were less susceptible to diabetes.
However, other strains developed a severe malfunction of fat and glucose metabolism as they continued to gain weight, causing them to rapidly develop type 2 diabetes.
The researchers say that this difference is due to a small fragment of genetic information: a so-called "jumping gene" or "transposon" of viral origin, localized in a non-coding segment of the gene Zfp69, whose effect it diminishes.
According to them, without this genetic fragment, the risk gene is fully active and, in combination with obesity, leads to high blood sugar levels and malfunction of fat metabolism.
They say that the gene is also active in the fat tissues of overweight people suffering from diabetes, more so than in healthy individuals.
"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," says first author Stephan Scherneck.
"We have therefore discovered a new diabetes gene of similar importance in mice and humans, as well as a mechanism that has not been described before in connection with the heredity of diabetes and obesity," says Hans-Georg Joost, head of the study and scientific director of the German Institute of Human Nutrition.
These data show the importance of studying in detail not only genes themselves, but also transposons in their vicinity.
Joost continued: "This transposon is quite active and almost completely "turns off" the Zfp69 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."
A research article on the findings has been published in the open-access journal PLoS Genetics.