Beta cell discovery could enhance diabetes treatment
Juvenile Diabetes Research Foundation-funded researchers at Stanford University have identified a pathway responsible for age-related decline in beta cells, and have shown they can tweak it to get older beta cells to act young again-and start dividing. These findings may help pave a path for developing strategies to restore beta cell number to treat both type 1 and type 2 diabetes.
As a person ages, the ability of their beta cells to divide and make new beta cells declines. By the time children reach the age of 10 to 12 years, the ability of their insulin-producing cells to replicate greatly diminishes. If these cells, called beta cells, are destroyed — as they are in type 1 diabetes — treatment with the hormone insulin becomes essential to regulate blood glucose levels and get energy from food.
In their work, the researchers, led by Seung Kim, M.D., Ph.D., of Stanford University, found that a protein called PDGF, or platelet derived growth factor, and its receptor send beta cells signals to start dividing via an intricate pathway that controls the levels of two proteins in the beta cell nucleus, where cell division occurs. Working with young mice, Dr. Kim and his team found that PDGF binds to its receptor on the beta cell’s surface and controls the level of these regulating proteins allowing cells to divide. However, in older mice, they discovered that beta cells lose PDGF receptors, and that this age-related change prevents beta cells from dividing. Dr. Kim and his colleagues further found that by artificially increasing the number of PDGF receptors, they can restore the ability of the beta cell to divide and generate new cells.
The work appears in the Oct. 12 issue of Nature.
To learn more, visit www.jdrf.org.