April 30 : Getting rid of those extra kilos may soon be just a pill away, for a boffin at the Salk Institute has developed a drug that chemically switches on PPAR-d, the master regulator that controls the ability of cells to burn fat.

Dr. Ronald M. Evans, who used the drug - a synthetic designed to mimic fat – on mice, also found that even when the rodents were not active, turning on the chemical switch activates the same fat-burning process that occurs during exercise.

The boffin now hopes that such metabolic trickery will lead to a new approach to new treatment and prevention of human metabolic syndrome.

Sometimes called syndrome X, human metabolic syndrome consists of obesity and the often dire health consequences of obesity: high blood pressure, high levels of fat in the blood, heart disease, and resistance to insulin and diabetes.

Dr. Evans had earlier discovered the role of the gene for PPAR-d, the master regulator of fat metabolism.

He found that by permanently turning on this delta switch in mice through genetic engineering, it was possible to create a mouse with an innate resistance to weight gain and twice the physical endurance of normal mice. Because they were able to run an hour longer than a normal mouse, they were dubbed “marathon mice.”

Subsequent work in the Evans laboratory found that activation of PPAR-d in these mice also suppresses the inflammatory response associated with arthrosclerosis.

However, the reason why Dr Evans is so excited about chemical metabolic engineering is because it offers help to an adult whose muscles are already formed and who now would benefit greatly from having more active, fat-burning muscles.

Genetic metabolic engineering that created the marathon mouse was turned out before birth.

Dr Evans believes that having access to an “exercise pill” would improve the quality of muscles, since muscles like to be exercised, and increase the burning of energy or excess fat in the body.

This would also result in less fatty tissue, lower amounts of fat circulating in the blood, lower blood glucose levels and less resistance to insulin, lowering the risks of heart disease and diabetes.

The ability to chemically engineer changes in metabolism also has given the researchers more insight into how the PPAR-d switch works, says Dr. Evans. Genetically engineering changes in metabolism in the marathon mice triggers both increased fat burning and increased endurance. Adult normal mice that receive the drug to switch on PPAR-d show increased fat burning and resistance to weight gain, but they do not show increased endurance.

This suggests the delta switch can operate in different modes, and the laboratory is in the process of figuring out exactly how.

Dr. Evans presented his drug at the Experimental Biology 2007 in Washington, DC. (ANI)