A natural process by which the beta cells of the pancreas, which make and secrete insulin, create new beta cells. Diabetes researchers are keenly interested in exploiting the mechanisms behind this phenomenon to some day prevent, treat, or cure Type 1 diabetes.
It has been known for some time that mammals (including humans) eventually regenerate some types of cells to replace injured cells. There is now growing evidence that we have some ability to regenerate beta cells. In pregnant or obese individuals, for example, the mass and number of beta cells expand considerably to meet the body’s increased insulin requirements.
Beta-cell regeneration raises tantalizing possibilities for the treatment of Type 1 diabetes. The autoimmune destruction of beta cells is gradual, and recent research suggests that many people with long-standing diabetes still appear to have some residual beta-cell function, sometimes even decades after diagnosis. The body’s natural regeneration of beta cells may be hampered by high blood glucose levels, which can damage newly regenerated beta cells, and by the autoimmune process that caused diabetes in the first place.
If researchers could intensify blood glucose control, learn how to turn off the autoimmune response, and give people something that would stimulate beta-cell growth, perhaps regeneration and restoration of functional beta-cell mass might occur, even in people with established Type 1 diabetes. Alternatively, perhaps people in the very earliest stages of Type 1 diabetes could be treated to delay the onset of — or prevent — full-blown clinical diabetes.
Understanding beta-cell regeneration could be a boon to islet transplantation as well. The success of the Edmonton Protocol has shown that islet transplantation can essentially restore insulin independence in individuals with Type 1 diabetes for several years. However, there are not nearly enough donor pancreases available each year to provide islets to everyone who could benefit from an islet transplant. In many cases, it takes multiple donor organs to induce insulin independence in a single transplant recipient. Ideally, this problem could be solved by exploiting the principles of beta-cell regeneration to grow large numbers of functional beta cells from donor organs in tissue culture and then transplanting the expanded beta cells. At the very least, researchers hope that beta-cell regeneration could be used to enhance currently used islet transplantation methods.
Researchers are eager to identify and study substances that can be used to stimulate beta-cell regeneration. One key player is a hormone called glucagon-like peptide-1 (GLP-1). GLP-1 has a number of positive effects in diabetes, including the regeneration of beta cells, protection of those cells against apoptosis (programmed cell death), enhancement of insulin secretion after meals, and suppression of the release of glucose from the liver after meals. A number of pharmaceutical companies are now developing and testing long-acting analogs of GLP-1 in both Type 1 and Type 2 diabetes. In fact, a synthetic, longer-acting GLP-1-like molecule called exenatide, marketed by Amylin Pharmaceuticals and Eli Lilly and Company as Byetta, received approval from the U.S. Food and Drug Administration in April 2005 as an adjunctive treatment for Type 2 diabetes.
The National Institute of Diabetes and Digestive and Kidney Diseases is sponsoring a clinical trial to study the effects of exenatide in people who have had Type 1 diabetes for at least five years but whose pancreases still make some insulin. The trial is designed to determine whether exenatide can improve the pancreas’s ability to make insulin and help control blood glucose. Other researchers also plan to study whether giving GLP-1 or GLP-1 analogs to people receiving islet transplants can improve the success rate of transplantation.