Hamburg - A team of German scientists may have discovered two new genes which can "switch off" type 2 diabetes, which strikes millions of people as they get older. The German researchers have identified one gene associated with a higher risk of diabetes, as well as a "jumping gene" which appears to disrupt its activity, thus helping to reduce the risk of diabetes.
The findings, published in the journal Public Library of Science (PLoS) Genetics, are the first real hope for the 230 million people worldwide with type 2 diabetes.
The risk of developing the condition depends partly on lifestyle factors, such as being overweight, and partly on a person's genetic makeup.
In recent years, scientists have identified a number of genes that influence the likelihood of a person developing type 2 diabetes.
In this latest study, German scientists identified a gene called Zfp69 as being a risk factor for diabetes in mice.
Also, the corresponding human gene (ZNF642) was found to be particularly active in overweight people with diabetes. According to the researchers, Zfp69 codes for a protein that appears to interfere with the storage of fat in fatty tissues, and so enhances the deposition of fat in the liver.
"Our data suggest that the protein product of the risk gene in obese individuals enhances the storage of fat in fat cells," explained the lead author of the paper, Dr Stephan Scherneck of the Department of Pharmacology at the German Institute of Human Nutrition (DIfE).
"As a result, excessive fat accumulates in the liver and this in turn contributes to the development of diabetes."
The scientists also compared two strains of mice: one had problems with fat and glucose metabolism and rapidly developed type 2 diabetes, and the other was obese but less susceptible to diabetes.
The difference between the two was the presence of a so-called "jumping gene" or transposon in the Zfp69 gene in the non-diabetic mice. Transposons are small stretches of DNA which are able to "jump" around the genome.
In this case, the transposon effectively "switches off" the gene and so reduces the diabetes risk in mice.
"We have therefore discovered a mechanism that has not been described before in connection with the heredity of diabetes and obesity," said Hans-Georg Joost, scientific director of the DIfE.
The researchers suggest that in the future, studies should pay greater attention not only to genes but also to transposons in their vicinity.
