Rare mutations in a gene called SLC30A8 lower diabetes type-2 risk by 65 percent, researchers have found.
The mutations were seen in people with different ethnicities, meaning that a drug designed to mimic the protective effects of these mutations could protect people around the world from diabetes.
The latest study was conducted by researchers at Broad Institute and Massachusetts General Hospital (MGH). It was based on data from 150,000 people from U.S., Iceland, Sweden and Finland, according to Bloomberg.
Diabetes type-2 is a condition when the body can't control the levels of glucose in the blood.
The mutations in SLC30A8 can protect even at-risk groups (old or overweight) from the disease. Inheriting one copy of the defective gene is enough to lower diabetes type-2 risk by 65 percent, researchers found.
"This work underscores that human genetics is not just a tool for understanding biology: it can also powerfully inform drug discovery by addressing one of the most challenging and important questions - knowing which targets to go after," said David Altshuler, at Massachusetts General Hospital, one of the study authors.
Altshuler and colleagues found that the defective genes disrupt the function of the protein ZnT8. The protein transports zinc into insulin-producing beta cells. Researchers aren't sure how the lower levels of ZnT8 protect against diabetes.
According to the researchers, inhibiting activity of protein ZnT8 could be a good way of targeting diabetes type-2.
Pharmaceutical giant, Pfizer Inc. has also funded the current research and might have an advantage over rival drugmakers in developing a drug that prevents diabetes, Bloomberg reported.
Previous research had shown that the protein encoded by SLC30A8 is associated with diabetes type-2. Mice studies showed that the gene SLC30A8 variants might increase rather than decrease the diabetes risk.
However, researchers in the present study found that the gene mutations have opposite effects in humans. Altshuler told the New York Times that the group's first paper describing the protective role of SLC30A8 mutations in humans was rejected because one of the reviewers said that it contradicted the results of a study on the gene conducted on mice.
The study is published in the journal Nature Genetics.
Funding for the study came from Pfizer, the National Institutes of Health, the Doris Duke Charitable Foundation and others.
Over 300 million people around the world and 26.9 million adults in the U.S. suffer from diabetes type-2. Health experts believe that the number of people with the condition is expected to rise in the future due to poor lifestyle and lack of exercise, meaning that the market for drugs that promise to prevent the disease is quite promising.