Medical Breakthroughs for Weight Loss: Managing Your Midsection

Managing Your Midsection

Keeping your weight down is a critical factor in controlling type 2 diabetes, but much about how the body regulates appetite, metabolism, fat accumulation, and other factors isn't well understood. As rates of obesity in the United States continue to climb along with rates of Diabetes, the government has launched public-education campaigns to bring attention to the dangers of obesity. In the meantime, researchers are working to create new tools for managing your midsection.

The main principles of weight loss remain the same: To lose pounds, you need to burn more calories than you take in. But many people find this difficult because the body seems programmed to keep weight consistent. Much of the research into obesity seeks to understand just how the body's internal controls work. Here are some recent insights.

Finding "fat" genes. What you do (or don't do) has a lot to do with how much you weigh, but it's also clear that fatness runs in families. By some estimates, as much as 40 to 70 percent of such traits as body mass and fat formation in the gut are determined by your genes. Now that the human genome has been mapped, scientists are trying to zero in on the genes -- and there are likely to be many -- that contribute to weight control. One exciting development was the discovery of a genetic defect that curbed production of a newly identified appetite-regulating hormone called leptin. Now researchers are looking at clusters of genes on two different chromosomes that may predispose people to abdominal fat and insulin resistance. The hope is to determine how the relevant genes interact with each other and eventually be able to custom-design drugs that can fix fat-affecting flaws in an individual's genetic makeup.

Leveraging leptin. Genetic defects may not be the most important influence on leptin. In fact, most obese people have ample amounts of the hormone but don't seem to benefit from its ability to signal when appetite is satisfied. Researchers aren't sure why, but they may now have another piece of the puzzle. In an exciting development at Harvard's Beth Israel Deaconess Medical Center, scientists have identified a protein that appears to help regulate signals that allow leptin to work. The protein has two important effects: It makes lab mice stay slim, even when they are fed a high-fat diet, and it boosts insulin sensitivity. This makes the protein, called PTP1B (protein tyrosine phosphatase 1B), a potentially powerful agent against both obesity and type 2 diabetes. This research, funded by both the National Institutes of health and the American Diabetes Association, has not yet gone beyond animal testing, but it provides an intriguing basis for further study.

Suppressing the appetite. Everyone dreams of a safe pill that would act as a switch to turn off appetite. But it's unlikely that a single chemical agent will do the trick because the urge to eat is regulated by a complex biochemical process with many players. Still, researchers are working to identify the players in hopes of tackling a few of them to give dieters an edge.One candidate described recently in the British science journal Nature is a molecule called OEA (oleylethanolamide). Levels of OEA in the intestine increase when you eat. Scientists believe the compound helps trigger feelings of fullness that make you stop eating. In studies at the University of California, rats that were given OEA reduced their food intake and their weight. A chemically similar drug developed by a French company is now being tested in people.

Another prospect is a compound called C75, which appears to curb appetite by affecting several brain chemicals at once. Obese lab rats injected with C75 ate less even after fasting, according to a study at Johns Hopkins University School of Medicine. What's more, the compound seems to increase metabolism to make animals burn more energy -- meaning it may boost weight loss by both cutting and burning calories. Drug tests in people are likely within three years.

Obesity and the Brain

If you remember the high-fashion emaciated look known as "heroin chic," then you have a picture of what narcotics do besides blow your mind: They curb the appetite and make you lose weight. Wasting your mind and body is hardly a path to good health, but the link between weight loss and pleasure-producing chemicals in the brain hasn't been lost on scientists. Of particular interest is dopamine, a neurotransmitter produced when you satisfy urges like sex and eating. Brain researchers at Brookhaven National Laboratory have found that obese people have fewer sites, or receptors, on cells for dopamine to dock with than normal-weight people. The scientists speculate that overeating may be caused by a greater need for stimulation to produce satisfaction. Implication: Other activities that boost dopamine in the brain -- such as exercise -- can take the edge off cravings.

Other studies by the same researchers indicate another difference in obese people: Areas of the brain that process sensual signals about food from the mouth, lips, and tongue are more active than they are in normal-weight people. This raises the possibility that drugs that make food less palatable may help people lose weight despite sensory hot spots in the brain.