"These findings are important because, in diabetes, beta cells in the pancreas have a limited if any capacity to proliferate, and they die at a steady rate," says Joel Habener, MD, of the MGH Laboratory of Molecular Endocrinology and an investigator with the Howard Hughes Medical Institute, the paper?s senior author.
Type 1 diabetes is caused by destruction of insulin-producing beta cells of the pancreas in a mistaken attack by the body?s immune system. As a result, patients do not produce the insulin required for proper glucose metabolism and need to take insulin injections. In type 2 diabetes, the most common form of the disease, patient' beta cells do not produce enough insulin at the right time during a meal, and their overall metabolism does not respond correctly to insulin. As a result, their blood glucose levels rise. This so-called hyperglycemia can exert further deleterious effects on beta cells. For both types of diabetes, finding new ways to provide functioning beta cells has been an area of great interest for researchers.
One current strategy being explored for treating type 1 diabetes is transplantation of beta cells, but these cells are in limited supply and may be rejected by the patients' immune systems. Therefore, finding alternative sources of insulin-secreting cells is necessary.
Clinical trials have shown that an intestinal hormone called glucagon-like peptide-1 (GLP-1) can provoke beta cells to proliferate and to secrete insulin. Habener and his laboratory now provide evidence that the hormone may also cause islet stem cells to d
Contact: Susan McGreevey
Massachusetts General Hospital