Hungry or full, fat or thin: It is mostly a matter of hormones, dozens of them, carrying messages between the digestive tract, the fat cells and the brain. Eat. Don't eat. Burn calories. Store fat.

On Friday, researchers at Stanford University reported that they have found a previously unknown member of this chemical cascade, a hormone with a much-coveted power: It sharply reduces the desire to eat.

The new substance, which the scientists named obestatin (OHB-statin), is made in the stomach and small intestine, and it seems to prompt the brain to send out a signal that says "eat less."

Mice given the hormone for eight days ate half as much as usual and lost weight, the researchers reported in the journal Science. The hormone seems to reduce hunger in part by slowing the passage of food through the stomach and small intestine.

The study's director, Dr. Aaron Hsueh, said obestatin had not been studied in people and had been tested only in mice.

But Stanford issued a statement saying Johnson & Johnson, which sponsored the research, has rights to the discovery. With obesity rates shooting up worldwide, drug companies are scrambling to develop weight-loss drugs, especially appetite suppressants.

Dr. David E. Cummings, an obesity researcher at the University of Washington, Seattle, who was not involved in the obestatin study, said, "The chances that this is going to hold up in humans are very high."

But it is not clear how strong a role the molecule plays in weight control or whether it could lead to a new drug. To be used as a drug, obestatin would have to be injected or perhaps made into a nose spray. It could not be taken in pill form because it would be broken down in the stomach.

People dislike injections, so drug companies are more likely to try to develop a molecule that mimics obestatin but can be taken by mouth, said Dr. Rudolph Leibel, an obesity researcher at Columbia University.

In an essay accompanying the report in Science, another obesity expert, Dr. Matthias Tschoep, from the University of Cincinnati, wrote that obestatin's "effect on body weight appears to be subtle."

Although mice given the hormone eat less, they do not lose as much weight as would be expected. Tests also suggest that the weight they do lose might not be fat. If the drug makes muscles shrink, that would be undesirable, Tschoep said in an interview.

But the molecule has been studied only in normal mice, not fat ones. Also unknown is what a mouse feels like on obestatin. Does the hormone simply diminish appetite — or make the animal feel sick? The answer is not obvious, because rodents do not vomit. A drug that produced weight loss by making people throw up might not be a good idea.

Tschoep wrote, "The search for a magic bullet against obesity is likely to continue."

Other researchers are eager to study the molecule. Cummings said that as soon as he heard about it he began trying to reach Hsueh to propose that they work together to measure its levels in humans.

One thing that especially fascinates scientists about obestatin is its link to another hormone, ghrelin, which makes people hungry — the opposite of obestatin.

The scientists were surprised to find that the two hormones were products of the same gene. The gene directs cells to make one protein molecule, which breaks into two smaller ones, called peptides. One is ghrelin, and the other is obestatin.

The same gene is found in at least 11 species of mammals, Hsueh and his colleagues reported, indicating that its role in controlling food intake must be important for survival.

But Leibel said having two hormones with opposite effects embedded in the same molecule was like driving with one foot on the brake and one on the gas.

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"One might wonder, why would you do this?" he said. "Why design a system like this?"

Finding the answer will require more research.

The hormone's existence helps explain something that has been puzzling scientists about ghrelin, Cummings said. When scientists created a mouse lacking the ghrelin gene they expected it to be extremely skinny and lack interest in food. Instead, the mice were nearly normal.

Friday's discovery may explain why: Although deleting the gene took away ghrelin, the hunger signal, it also took away obestatin, the fullness signal. The deletion wound up having no net effect.

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