31 March 2008
ByAppeared in BioNews 451
US and European scientists have identified six more genes that play a role in Type 2 diabetes, bringing the total number of genetic variations associated with the disease to 16. The research, published in the journal Nature Genetics, combined the results of three earlier studies carried out on over 10,000 people. Follow-up experiments then confirmed that particular versions of the JAZF1, CDC123-CAMK1D, TSPAN8-LGR5, THADA, ADAMTS9 and NOTCH2 genes confer an increased risk of Type 2 diabetes.
Type 2 diabetes affects over 170 million people worldwide. People with diabetes cannot regulate their blood sugar levels properly, either because their pancreas is not making enough insulin, or because the body becomes resistant to its effects. Type 2 diabetes usually affects people over the age of 40. It is more common in overweight, inactive people, and those with a family history of the disease.
The latest findings will shed light on the processes that go wrong in diabetes, paving the way for new approaches to preventing and treating the disease, say the researchers. 'None of the genes we have found was previously on the radar screen of diabetes researchers', said Professor Mark McCarthy, co-leader of the study.
Interestingly, one of the newly discovered genes - JAZF1 - is also known to play a role in prostate cancer. People who inherit two copies of a particular variant of this gene have a 30 per cent increased chance of developing diabetes, while a different version of the same gene appears to increase the risk of prostate cancer. It seems that for JAZF1, as well as at least two other genes identified last year, a raised risk of diabetes is probably 'balanced' by a reduced risk of cancer.
Professor McCarthy said that while one such 'seesaw' gene could be a fluke, the fact that three have so far been discovered makes it more likely that the biological mechanisms underlying the two diseases are connected. One explanation could be that gene variants that trigger increased cell multiplication protect against diabetes, as they could help the pancreas make more insulin-producing beta cells. However, these same variants could increase the risk of cancer, which is essentially the uncontrolled growth and multiplication of cells. 'Put bluntly, too great a tendency fro cell cycle and cell division would tend to predispose to cancer, and too little towards diabetes', said McCarthy.
Dr Jess Buxton is Contributing Editor at BioNews and a Trustee at the charity that publishes it, the Progress Educational Trust (PET). She is co-author of The Rough Guide to Genes and Cloning (buy this book from Amazon UK) and Human Fertilisation and Embryology: Reproducing Regulation (buy this book from Amazon UK).