An international team of scientists has identified six new genes associated with type 2 diabetes, raising to 16 the total number of genes found to be implicated in diabetes. Intriguingly, one
of the newly identified genes has also been shown to play a role in the development of prostate cancer.

‘None of the genes we have found was previously on the radar screen of diabetes researchers,’ commented Professor Mark McCarthy of the University of Oxford in the UK. ‘Each of these genes
therefore provides new clues to the processes that go wrong when diabetes develops, and each provides an opportunity for the generation of new approaches for treating or preventing this
condition.’

Over 200 million people around the world suffer from type 2 diabetes, which is characterised by a breakdown in the systems which control blood sugar levels, leading to abnormally high levels of
glucose in the blood. Exposure to high levels of glucose over many years is damaging to our vital organs, and in many countries type 2 diabetes is a leading cause of heart disease and stroke as
well as blindness, kidney failure and amputations not related to accidents.

It most commonly affects overweight, sedentary people over the age of 40, although recent years have seen growing numbers of younger people developing the disease.

In this latest study, over 90 researchers from more than 40 centres in Europe and the US analysed genetic data from some 70,000 people in the hunt for small differences in the genetic code
which could make some people more susceptible to developing type 2 diabetes than others. The work, which was partly funded by the EU, is published online in the journal Nature Genetics.

In total the scientists were able to identify six genetic variants associated with an increased risk of type 2 diabetes. The findings support previous research which suggests that a major
element in the development of type 2 diabetes is a failure to regulate the number of insulin-producing cells in the pancreas.

‘These new variants, along with other recent genetic findings, provide a window into disease causation that may be our best hope for the next generation of therapeutics,’ said Francis S
Collins, Director of the National Human Genome Research Institute in the US. ‘By pinpointing particular pathways involved in diabetes risk, these discoveries can empower new approaches to
understanding environmental influences and to the development of new, more precisely targeted drugs.’

The researchers underline the fact that each of these genes only increases the risk of developing type 2 diabetes by a small amount, and although their combined effects may be stronger, it is
likely to be some time before genetic testing can be used to give predictions of disease risk in individual patients.

‘Once we more fully understand the large numbers of genes now implicated in diabetes risk, it might become possible to identify people at particularly high risk before the disease takes root,’
explained Professor David Altshuler of the Broad Institute of Harvard and the Massachusetts Institute of Technology (MIT) in the US. ‘However, until we have evidence that using such information
results in better health outcomes, widespread genetic testing would be premature.’

One surprise thrown up by the results was the finding that one of the genes found to be implicated in diabetes, JAZF1, has also been shown to play a role in prostate cancer. In fact JAZF1 is
the second gene to be linked to both diseases; earlier research revealed that a single variant of a gene called HNF1B is associated with an increased risk of diabetes but a decreased risk of
prostate cancer. In the case of JAZF1, the diabetes and prostate cancer variants are found in different parts of the gene and there is no known relationship between them.

‘Genetic studies of this kind are revealing new and unsuspected connections between diseases,’ said Dr Eleftheria Zeggini of the University of Oxford. ‘This is now the second example of a gene
which affects both type 2 diabetes and prostate cancer. We don’t yet know what the connections are, but this has important implications for the future design of drugs for these conditions.’

EU support for the research came from the EU-funded EURODIA (‘Functional genomics of pancreatic beta cells and of tissues involved in control of the endocrine pancreas for prevention and
treatment of type 2 diabetes’) and EUGENE2 (‘European network on functional genomics of type 2 diabetes’), both of which are financed through the ‘Life sciences, genomics and biotechnology for
health’ thematic area of the Sixth Framework Programme (FP6).

For more information, please visit:
http://www.nature.com/naturegenetics
http://www.wellcome.ac.uk