BOSTON -- April 2, 2007 -- A new Joslin-led study has identified the insulin receptor as an important protein that promotes islet cell growth in mice whose bodies are unable to use insulin properly, or are insulin resistant, a precursor to type 2 diabetes. Since the body's natural response to insulin resistance is to increase insulin secretion from the pancreas and grow more islet cells, also known as beta cells, harnessing this growth response could lead to new treatments for type 2 diabetes. The study appears in the early online edition of this week's Proceedings of the National Academy of Sciences.
"The failure to grow more functional beta cells (also called compensatory islet cell growth response) leads to overt diabetes," said Rohit N. Kulkarni, M.D., Ph.D., Investigator at Joslin Diabetes Center and Assistant Professor of Medicine at Harvard Medical School, who led the study. "If we can identify the key signaling proteins critical for the islet cell growth response, we can develop potential therapeutic targets to enhance the growth of beta cells."
There are two proteins that mediate the effects of growth factors in beta cells, the insulin-producing cells in the pancreas: insulin receptor, a protein that mediates the action of insulin, and IGF-1 receptor, another protein that closely resembles the insulin receptor and mediates the action of insulin-like-growth factor (IGF-I), a hormone and growth factor. These two receptors have been a major focus of research studies by Dr. Kulkarni and others at Joslin Diabetes Center who want to better understand beta cell growth and functioning so that these essential cells can be increased in people with diabetes.
In type 2 diabetes, the body doesn't produce enough insulin and/or is unable to use insulin properly (insulin resistance). This form of diabetes usually occurs in people who are over 40, overweight, and have a family history of diabetes, although today it is increasingly occurring
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Contact: Jenny Eriksen
jenny.eriksen@joslin.harvard.edu
617-732-2415
Joslin Diabetes Center
2-Apr-2007