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17 April 2014 12:48 pm ,
Vol. 344 ,
Officials last week revealed that the U.S. contribution to ITER could cost $3.9 billion by 2034—roughly four times the...
An experimental hepatitis B drug that looked safe in animal trials tragically killed five of 15 patients in 1993. Now,...
Using the two high-quality genomes that exist for Neandertals and Denisovans, researchers find clues to gene activity...
A new report from the Intergovernmental Panel on Climate Change (IPCC) concludes that humanity has done little to slow...
Astronomers have discovered an Earth-sized planet in the habitable zone of a red dwarf—a star cooler than the sun—500...
Three years ago, Jennifer Francis of Rutgers University proposed that a warming Arctic was altering the behavior of the...
- 17 April 2014 12:48 pm , Vol. 344 , #6181
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Possible Gene for Adult-Onset Diabetes
3 January 2001 7:00 pm
Researchers have stumbled upon a gene that may underlie some cases of adult-onset diabetes. If so, the discovery could eventually lead to better treatments and diagnostic tests.
In adult-onset diabetes, cells don't respond well to insulin, a hormone that normally tells them to absorb and store glucose. Most adults who develop type II diabetes are chronically underactive and overweight, so current treatments include changes to diet and more exercise, and sometimes drugs and insulin injections. But these approaches often can't prevent diabetes-related damage to the heart, kidneys, nerves, and blood vessels. Researchers hope that by identifying genes that contribute to the disease, they may be able to develop better therapies. Genetic screening might also help people at risk ward off the disease. So far, however, the handful of implicated genes accounts for only 5% to 10% of the cases.
Now a new, unexpected candidate has come to light. A team led by molecular biologist Stephane Schurmans of IRIBHN in Gosselies, Belgium, had engineered mice to lack a gene that appeared to be a tumor suppressor. But mice without this gene, called SHIP2, didn't get cancer. Instead, they had difficulty breathing, turned blue, and died within 3 days of birth--telltale symptoms of hypoglycemia, or low levels of blood sugar, the researchers report in the 4 January issue of Nature.
The researchers found that the mice develop a hypersensitivity to insulin. This is not diabetes, in which people respond sluggishly to insulin. But Schurmans suggests that because SHIP2 seems to govern sensitivity to insulin, it's possible that some forms of the gene may reduce responsiveness to the hormone, causing the insulin resistance that is the hallmark of diabetes. If so, he says, drugs that inhibit the mutated gene might ease symptoms, and genetic tests might uncover susceptible people before the disease develops.
The study "moves this gene higher up on the list of candidates for diabetes," says Clifton Bogardus of the National Institute of Diabetes and Digestive and Kidney Diseases in Phoenix, Arizona. But he cautions that many possible diabetes genes have never panned out, and the link will be theoretical until a SHIP2 mutation turns up in human diabetics--something that the researchers have already begun to search for, Schurmans says.