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WEDNESDAY, June 7 (HealthDay News) -- New animal research suggests that a naturally produced estrogen hormone known as estradiol might help protect against diabetes by preventing the death of pancreatic cells critical to the production of insulin.
The findings are based on work with mice and have not yet been tried in a human trial.
"This is the first study that shows that the female hormone estrodial is important to ensuring pancreatic beta-cell survival in both females and males," said study co-author Dr. Franck Mauvais-Jarvis. He is an assistant professor with the department of molecular and cellular biology and the department of medicine in the division of diabetes, endocrinology & metabolism at Baylor College of Medicine in Houston.
Most people with diabetes have what's known as the type 2 form of the disease, which results from the body's inability to properly use the naturally produced hormone insulin to regulate blood sugar levels by processing sugars into energy.
However, between 5 percent and 10 percent of diabetics have a version of the disease known as type 1 diabetes, in which the body doesn't produce any insulin.
Focusing on type 1 diabetes, Mauvais-Jarvis and his colleagues noted that the body's inability to produce insulin is driven by the death of insulin-producing pancreatic beta-cells.
In an attempt to isolate estradiol's potential impact on pancreatic beta-cell destruction, the researchers worked with both male and female mice that were either unable to produce estradiol, lacked an estrogen receptor needed for normal estradiol functioning, or were given a compound that prevented the estrogen receptors from working.
Reporting in this week's issue of the Proceedings of the National Academy of Sciences, the researchers said that both genders of mice experienced severe beta-cell death while demonstrating dramatically lower-than-normal levels of insulin production -- leading to the onset of type 1 diabetes.
However, Mauvais-Jarvis and his team found that after administering targeted doses of estradiol, the pancreatic beta-cells were "rescued" from death, insulin production resumed, and diabetes was averted.
The researchers concluded that -- at least in mice -- estradiol appears to offer protection against the chain of events that lead to type 1 diabetes.
Mauvais-Jarvis was cautiously optimistic that the work with mice might one day translate into a benefit for humans at risk for diabetes.
"One has to be cautious, because this study has been performed in mice, and although the mouse is the best available model to study human diseases, mice are not humans," he said.
Still, Mauvais-Jarvis said the study indicates that estradiol may offer a new clinical route for the prevention of diabetes in women and men.
"That's a novel paradigm," he said. "Thirty years ago, it was believed that sex hormones were involved only in reproduction and sexual behavior. But in the last 10 years, there has been a kind of challenge to this concept, and we have discovered novel functions regarding estrodial -- such as the prevention of beta-cell death -- that have been revealed to be true for both sexes."
Mauvais-Jarvis stressed, however, that offering patients estrogen-replacement therapy wasn't an option, given recent findings that such treatment appears to elevate the risk of breast cancer in women.
Rather, he suggested that "the future is try to dissect the good and the bad uses of estrodial," in an effort to develop medicines that could prevent beta-cell deaths and diabetes without harmful side effects.
Dr. Robert Rizza, a professor of medicine at the Mayo Clinic, and president of the American Diabetes Association, called the new findings "intriguing."
"There have been various studies that have shown that estrogen may lower the risk for developing diabetes, and this study shows why this might be the case," he sad. "This could be a mechanism."
"It may or may not be true for humans," Rizza added. "But it will teach us more about how estrogen works. And if it turns out to be the case, this could be used for other novel therapies to prevent diabetes."
SOURCES: Franck Mauvais-Jarvis, M.D., Ph.D., assistant professor, department of medicine, division of diabetes, endocrinology & metabolism and department of molecular and cellular biology, Baylor College of Medicine, Houston; Robert Rizza, M.D., professor, medicine, Mayo Clinic, Rochester, Minn., and president, American Diabetes Association; June 5-9, 2006, Proceedings of the National Academy of Sciences
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