Japanese scientists believe they may have found an antidote for a sweet tooth.

A hormone called leptin, released by fat cells in the body, has been found to suppress cravings for sweet and sugary food, at least in mice.

After being released into the bloodstream, leptin is known to act on a part of the brain called the hypothalamus, where it carries a message to stop eating.

This is the first evidence that leptin also affects a taste for sugary substances by acting on sweet-tasting receptors in the tongue.

Writing in the journal Proceedings of the National Academy of Sciences, the scientists say they think leptin may act in the body as a sort of sweet tooth suppresser, helping to regulate the intake of food.

But so far, the experiments have only been carried out on rodents.

Born to be fat

The researchers from Tokyo Medical and Dental University, Asahi University School of Dentistry, the Japanese Ministry of Agriculture, Forestry, and Fisheries, and Kyushu University, Japan, gave leptin to both normal lean mice and to a strain of mice that had been bred to be genetically diabetic and extremely obese.

After being injected with leptin, the normal mice showed significantly smaller taste responses to sweets, but not salty, sour, or bitter substances.

However, genetically diabetic, extremely obese mice with defective leptin receptors continued to crave sweets after being given leptin.

The work raises the prospect of progress towards the "Holy Grail" of obesity research: an anti-fat pill.

But Keith Frayn, professor of human metabolism at Oxford University, UK, said there were important differences between rodents and humans in the way they respond to leptin - notably that leptin does not appear to increase energy expenditure in humans.

Anti-fat pill

"A pill that will enable you to eat as many sweets and cream buns as you like must be something that increases your expenditure of energy," Professor Frayn told BBC News Online.

"Leptin doesn't seem to do that in humans. What it's going to do is affect your appetite, stop you wanting to eat those sweets in the first place."

Early clinical trials of leptin in obese women had produced mixed results, he said. And if leptin were to be given in its natural form, it would have to be injected.

"People might not find that a tolerable way of improving a sweet tooth," he added.

"If it is going to be some non-protein sort of drug that will bind to the leptin receptor, that development is probably a good number of years away."