Stanford Scientists Discover Possible Target for Beta Cell Regrowth, as Reported by DiabeticLive.com

October 17, 2011

Scientists may someday be able to develop therapies that target this pathway to treat or prevent a variety of diseases, including diabetes as reported by DiabeticLive.com.

Orlando, FL (PRWEB) October 17, 2011

For those who have diabetes, there is hope for new treatments and possible a cure. A new molecular pathway related to the regeneration of beta cells in the pancreas has been discovered by a team of researchers at the Stanford University School of Medicine. Scientists may someday be able to develop therapies that target this pathway to treat or prevent a variety of diseases, including diabetes.

Sign up for a free glucose meter at DiabeticLive.com.

Published in the October 12 issue of “Nature,” the findings demonstrated that a molecule known as platelet-derived growth factor (PDGF) receptor activates a pathway linked to the production of pancreatic beta cells. The researchers found that as expression of the molecule decreases with age, so does regrowth of beta cells in the pancreas, which produce insulinâ”the hormone responsible for maintaining healthy levels of glucose in the blood by moving it into cells.

In young individuals, both in mice and humans, proliferation of pancreatic beta cells is maintained at a high level. However, as the individual ages, that production decreases significantly.

Scientists had previously identified a molecule called Ezh2 that was associated with the beta cell regrowth pathway; expression of the molecule decreased as beta cell production did the same. However, they were unsure of the mechanism that caused the reduction in expression of Ezh2.

The researchers in the Stanford study found that the reduction in PDFG receptor expression and slowing proliferation of pancreatic beta cells in juvenile mice appeared to be related, as they followed a similar pattern.

They demonstrated the link when they blocked expression of PDGF receptors in juvenile lab mice, which caused a decrease in production of Ezh2. Meanwhile, control animals showed no changes in expression of PDGF receptors. The mice producing less Ezh2 displayed higher blood glucose levels than controls and were also unable to remove glucose from the bloodstream as efficiently as controls.

Inhibiting the expression of PDGF receptors affected adult mice, too: they were much less able to replace beta cells that were destroyed by a chemical compound administered by the researchers, and they developed diabetes soon after.

Dr. Seung Kim. M.D., Ph.D., was the senior author on the study. Kim is hopeful that the findings will allow scientists to develop therapies for diabetes based on the activation of the pathway. “We’re hopeful that soon we might be able to manipulate this pathway in a therapeutic way in humans,” said Dr. Kim.

“Perhaps by rekindling its expression and then activating it through a drug we could give in an injection or through some other route. This could be a kind of one-two punch against diabetes,” he continued.

Get a free diabetic life insurance quote from DiabeticLive.com.


For the original version on PRWeb visit: http://www.prweb.com/releases/prwebDiabetes/Beta-Cells/prweb8883930.htm

Source: prweb

comments powered by Disqus