Altering Single Gene in the Brain of Mice Cures Abnormal Sugar Metabolism Seen in Type 2 Diabetes.
A new study shows that altering a single gene in the brains of obese mice bred to have type 2 diabetes helped them completely normalize blood sugar levels. So quite literally the key to curing type 2 diabetes may be all in our heads, or at least until further research and human trials, in the heads of mice Researchers have claimed that this is the first study that indicates glucose control may be regulated by the brain. If continued research further supports these findings, it could open a whole new approach to treating type 2 diabetes and considerable hope to those with the condition. People with type 2 diabetes are unable to regulate their blood sugar (glucose) levels normally because their bodies have become resistant to insulin, which is the hormone responsible for controlling glucose in the blood. Researchers say that obesity is thought to lead to decreased insulin sensitivity and then to type 2 diabetes. But this study suggests that obesity and type 2 diabetes may both be caused by the same genetic defect in the brain. Brain Gene Provides Glucose Control: In the study, published in the November issue of Diabetes, researchers looked at the effect of manipulating a gene in the brain known as POMC in mice bred to be obese with type 2 diabetes. Previous studies have shown that POMC production is reduced in the brains of obese and diabetic mice. People with mutations in this gene are also obese and diabetic. But because many genes are implicated in obesity and diabetes, it’s not clear which genes, if any, play a role in regulating glucose levels. The study showed that when the activity of POMC was increased through genetic engineering, the mice reduced their food intake slightly and lost some weight. “But the surprising part was that the effect on glucose regulation was not partial,” says researcher Charles V. Mobbs, PhD, assistant professor at the Fishberg Neurobiology of Aging Laboratories at the Mount Sinai School of Medicine in New York City, in a news release. “Even though these mice remained obese, their glucose levels were completely normal.” Those findings showed that the dramatic improvement in glucose control and regulation was not related to the weight loss. New Direction for Diabetes Research: Mobbs says these new results suggest this perception of a cause-and-effect relationship between obesity and glucose control might sometimes be wrong. “It appears that both conditions can be caused by the same defects, impairments in the production, processing, or responsiveness to POMC gene products,” says Mobbs. Mobbs says it’s still too soon to rule out a role of obesity in glucose regulation, but drugs that mimic the effects of the POMC gene may eventually be useful for people who developed diabetes due to aging or as the result of damage to the hypothalamus, which might affect the body’s own POMC synthesis. He says drugs that mimic POMC are already being studied for the treatment of obesity, but it may turn out that these drugs will be even more effective in treating type 2 diabetes. But until those drugs are available, he says diet and exercise are the best way to control glucose levels and type 2 diabetes. (Source WebMD health news, Mizuno, T. Diabetes, November 2003; vol 52: pp 2675-2682. News release, Mount Sinai School of Medicine November 2003)