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An international team led by researchers at the Broad Institute and Massachusetts General Hospital (MGH) has identified mutations in a gene that can reduce the risk of developing type 2 diabetes, even in people who have risk factors such as obesity and old age.
Type 2 diabetes affects over 300 million people worldwide and is rising rapidly in prevalence. The current study breaks new ground in type 2 diabetes research and guides future therapeutic development in this disease.
The team identified a genetic mutation that appeared to abolish function of the SLC30A8 gene and that was enriched in non-diabetic individuals studied in Sweden and Finland. Then, in 2012, these unpublished results were shared with deCODE genetics, who uncovered a second mutation in an Icelandic population that also appeared to abolish function of the gene SLC30A8. Finally, the team set out to ask if the effects of SLC30A8 protective mutations were limited to the two mutations found in populations in Finland and Iceland. In laboratory experiments, members of Altshuler’s team showed that the protective mutations disrupt the normal function of the protein encoded by SLC30A8, known as ZnT8.
The work represents the fruits of a international collaborative effort among researchers from the Broad Institute, MGH, Pfizer Inc., Lund University, deCODE genetics and the T2D-GENES Consortium, which itself involves many universities and hospitals around the world.
Major funding for this work was provided by Pfizer Inc., National Institutes of Health, the Doris Duke Charitable Foundation, and others.
Founded by MIT, Harvard and its affiliated hospitals, and the visionary Los Angeles philanthropists Eli and Edythe L.
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The results focus the search for developing novel therapeutic strategies for type 2 diabetes; if a drug can be developed that mimics the protective effect of these mutations, it could open up new ways of preventing this devastating disease. Lifestyle changes and existing medicines slow the progression of the disease, but many patients are inadequately served by current treatments. In the new study, researchers describe the genetic analysis of 150,000 patients showing that rare mutations in a gene called SLC30A8 reduce risk of type 2 diabetes by 65 percent. Mutations in a gene called CCR5 were found to protect against infection with HIV, the virus that causes AIDS; drugs have been developed that block the CCR5 protein. The research team selected people with severe risk factors for diabetes, such as advanced age and obesity, who never developed the disease and in fact had normal blood sugar levels. The protection was surprising, because studies in mice had suggested that mutations in SLC30A8 might have the opposite effect - increasing rather than decreasing risk of type 2 diabetes.
That mutation independently reduced risk for type 2 diabetes and also lowered blood sugar in non-diabetics without any evident negative consequences.
As part of the NIH-funded T2D-GENES Project, chaired by Mike Boehnke at the University of Michigan, the Broad Institute had performed sequencing of 13,000 samples drawn from multiple ethnicities. The ZnT8 protein transports zinc into insulin-producing beta cells, where zinc plays a key role in the crystallization of insulin.
Broad Institute of Harvard and MIT was launched in 2004 to empower this generation of creative scientists to transform medicine. Broad, the Broad Institute includes faculty, professional staff and students from throughout the MIT and Harvard biomedical research communities and beyond, with collaborations spanning over a hundred private and public institutions in more than 40 countries worldwide. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $775 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.


The results were seen in patients from multiple ethnic groups, suggesting that a drug that mimics the effect of these mutations might have broad utility around the globe. A similar protective association for heart disease set off a race to discover new cholesterol-lowering drugs when mutations in the gene PCSK9 were found to lower cholesterol levels and heart disease risk. They focused on a set of genes previously identified as playing a role in type 2 diabetes and used next-generation sequencing (then a new technology) to search for rare mutations.
The T2D-GENES Project joined the collaboration, found ten more mutations in the same gene, and again saw a protective effect.
The protein encoded by SLC30A8 had previously been shown to play an important role in the insulin-secreting beta cells of the pancreas, and a common variant in that gene was known to slightly influence the risk of type 2 diabetes. The new type 2 diabetes study, which appears this week in Nature Genetics, suggests that CCR5 and PCSK9 are likely just the beginning but that it will take large numbers of samples and careful sleuthing to find additional genes with similar protective properties. Combining all the results confirmed that inheriting one copy of a defective version of SLC30A8 led to a 65 percent reduction in risk of diabetes. However, it was previously unclear whether inhibiting or activating the protein would be the best strategy for reducing disease risk - and how large an effect could be expected.



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