Stress Hormone's Startling Powers

A hormone that can wreak havoc with the body by setting off harmful effects of stress may have a far more positive use: in a new way to treat diabetes.

The hormone, known as corticotropin-releasing factor, or CRF, has been implicated in anxiety, obesity, addiction and even Alzheimer's disease. The brain and other organs make CRF. It triggers a cascade of chemicals that ultimately produce cortisol and adrenaline and activate the body's "fight or flight" response. Under chronic stress, cortisol breaks down muscle, suppresses the immune system and raises the risk of high blood pressure.

But recently, researchers have showed that CRF increases both insulin secretion and production of the cells that make insulin in the pancreas, known as beta cells. Diabetes, which affects nearly 24 million Americans, involves the body's inability to properly use insulin to convert sugar into usable energy. The findings, which support a hunch that others in the field have had, point to a possible pathway for treatment of diabetes.

"The machinery that allows the cell to respond to the hormone has been found," says Wylie Vale, a professor of molecular neurobiology at the La Jolla, Calif., Salk Institute for Biological Studies, who discovered the structure of CRF in 1981. "We are exploring how this machinery is controlled under conditions such as diabetes and obesity. What we really want to do is understand the system." The research of Dr. Vale and his colleagues was reported in a December paper published in the Proceedings of the National Academy of Sciences.

With Type 1 diabetes, formerly known as juvenile diabetes, the body doesn't produce enough insulin. This happens because the immune system attacks and kills beta cells. These patients are treated with insulin injections.

The most common form of diabetes, associated with obesity, is Type 2. Here, the body doesn't produce enough insulin and the cells from insulin-responsive tissues like muscle are unable to efficiently use the insulin that is produced. The beta cells go into overdrive to try to produce insulin but become overworked and ultimately stop functioning, according to Patricia Kilian, head of the beta-cell-regeneration program at the Juvenile Diabetes Research Foundation, which partially funded the study.