As a person ages, the ability of his or her 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 these insulin-producing cells to replicate greatly diminishes. If these beta cells are destroyed—as they are in type 1 diabetes—treatment with the hormone insulin becomes essential to regulate blood glucose levels and allow energy to be obtained from food. Now, longtime JDRF (Juvenile Diabetes Research Foundation)-funded researchers at Stanford University have identified a pathway responsible for this age-related decline, and have shown that they can manipulate it to make older beta cells act young again—and start dividing. The research, published online on October 12, 2011 in Nature, provides the most complete picture to date of the molecular and biochemical mechanisms that bring beta cell regeneration to a near halt as beta cells age. These findings may help pave a path for developing strategies to restore beta cell number to treat both type 1 and type 2 diabetes. In their study, the researchers, led by Dr. Seung Kim 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 is orchestrated. 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.
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