US scientists claim to have devised a drug that can switch on a gene to burn body fat, offering hope of an exercise pill.
And now pop a pill and burn away all the unwanted fat. The latest achievement of the scientists at The Salk Institute for Biological Studies, California in the US points in that direction.
Mice given the drug devised by them burned off fat, even when they did not exercise, and were resistant to weight gain despite a high-fat diet.
The Salk scientists assert though that the ultimate use of their drug would be to treat people at risk of obesity-related diseases like diabetes, rather than offer a "no-work six-pack" pill.
The drug mimics normal fat and chemically triggers a gene switch called PPAR-delta.
Turning on this switch activates the same fat-burning process that occurs during exercise.
Lead researcher Dr Ronald Evans believes the same will occur in humans.
UK expert Dr Fredrik Karpe, from the Oxford Centre for Diabetes, Endocrinology and Metabolism, is hoping to test this in the near future.
Commenting on the work, he said: "There has never been a method to 'medically' switch on fat burning before.
"The finding that PPAR-delta co-ordinates this process, not only by switching on fat burning, but also to rebuild the muscle in a way making it more fit for fat burning, is of major interest, not least as a completely novel approach for the treatment of the metabolic derangements accompanying obesity."
Many teams have been studying the genetic pathways controlling how muscle builds up and is broken down in the body.
Tests on rodents earlier too had showed that manipulating these pathways can halt muscle wastage from disuse or disease.
At least three research groups said they had identified some of the genes responsible.
Alfred Goldberg and colleagues at Harvard University in the US and a pharmaceutical company Regeneron said they had found genes called atrogin1 and muRF1 that were active during muscle wasting.
A team at Purdue University, Indiana, has been looking at a gene called erg1.
The drugs might mean that people with broken bones could avoid long and painful physiotherapy sessions to rebuild muscle strength.
Weaning people off respirators would also become easier as doctors could prevent wasting of the diaphragm.
National Aeronautics and Space Administration (NASA) of the US is also interested in the medicines because astronauts lose muscle mass on long missions.
Experts warn that although the drugs would maintain muscle size, they would not provide any of the other health benefits of regular exercise.
Professor Paul Greenhaff at Nottingham University in the UK who has been conducting similar research into muscle growth and wasting warned of the inherent potential for abuse in such drugs.
He said that the role of exercise had been underplayed.
"Contraction of the muscle itself is important. Exercise itself is the most highly potent stimulus of muscle growth. We must also look closer at nutrition as well."
Dr Julia Thomas at the Muscular Dystrophy Campaign said: "In order for this treatment to be truly beneficial it is important that muscle strength is also increased and future trials and research will be key in determining whether this is the case."
She said a pill to prevent muscle loss would unfortunately not be able to change the genetic cause of muscular dystrophy, but might slow down the disease progression.
"It is our hope that if this research becomes a workable drug the concentration of its use will be on serious medical conditions, such as muscular dystrophy, rather than for those desiring a 'gym in a bottle'."