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A lot is known about diabetes. But a discovery that could change how this disease is treated shows just how much more there is to learn.
A team of Harvard Medical School researchers has discovered a hormone made by liver and fat cells that signals the body to make more insulin-producing beta cells. A report of their work appears in this month’s issue of the prestigious scientific journal Cell.
For the team’s leader, Dr. Douglas Melton, research on the subject of diabetes is personal as well as professional. In 1993, his six-month-old son was diagnosed with type 1 diabetes. Since then Melton, who is co-director of the Harvard Stem Cell Institute, has turned his considerable research skills to learning how diabetes happens and how it might be cured.
In type 1 diabetes, the body’s immune system attacks the pancreas, a spongy little organ that sits below the stomach. The attack destroys insulin-producing cells in the pancreas, called beta cells. Without enough insulin, muscle cells can’t absorb sugar from the bloodstream. Sugar levels rise in the blood, causing havoc throughout the body. Untreated type 1 diabetes can be deadly. Even with treatment, usually daily injections of insulin, type 1 diabetes often leads to heart disease, vision problems, and nerve problems.
In the more common type 2 diabetes, the muscles resist that action of insulin, causing blood sugar to rise. As the pancreas churns out more and more insulin, the beta cells can eventually become burned out.
Over the years, Melton and his colleagues made a surprising discovery: the pancreas could make new beta cells, even in people with type 1 diabetes. “Old” pancreas cells can divide, forming young ones. Unfortunately, the pancreas isn’t naturally able to make enough new beta cells to make up for those killed by diabetes.
Melton and colleagues reasoned that there might be some chemical signal that prompts beta cells to divide and increase. The Cell paper details their search for and discovery of such a signal in mice. It’s a hormone the team called betatrophin. This hormone, made by liver and fat cells, travels through the blood to the pancreas. There, it prompts existing beta cells to grow and divide, making new beta cells.
In mice with diabetes, turning on the production of betatrophin by liver and fat cells caused an increase in beta cells and a dramatic improvement in blood sugar.
It will, of course, take much more research in mice—and then in humans—to determine if this newly discovered hormone can serve as a treatment for diabetes. So it’s too soon to get excited that the discovery of betatrophin will translate directly into a new treatment for diabetes.
This work is just the latest example of an even larger scientific discovery that has played out over the past two decades. We are learning that the human body has much greater power to naturally repair itself than we once imagined. Scientists all over the world are working to discover ways to stimulate the body’s own natural healing mechanisms, as Dr. Melton and colleagues are doing.
In the United States, this work and other important investigations are threatened by the “sequester,” which is cutting funding for medical research. It would be a shame for an important discovery like Melton’s to languish because of political infighting. Regardless of what you think about federal spending in general, if you share my view that we should not be cutting funding for health research and public health, you could do what I have done. Write your representatives in Congress to restore cuts in medical research.
