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They found a gene called PRDM16 in brown fat but not in white fat -- the type of fat found all over the bodies of most adult humans.

It may be possible to use this gene, or the protein whose production it controls, to help stop people from making too much white fat, the team at Harvard Medical School and the French research institute INSERM in Toulouse said.

"Brown fat is present in mice and in human infants, where it keeps them warm by dissipating food energy as heat, instead of storing it as white fat," said Dr. Bruce Spiegelman of Harvard's Dana Farber Cancer Center.

In humans, it all but disappears by adulthood, the researchers wrote in their report, published in the journal Cell Metabolism.

The question is whether humans can be taken back to an infantile state in which brown fat counteracts the buildup of white fat.

Spiegelman's team genetically engineered fat precursor cells with PRDM16 and injected them under the skin of mice.

The PRDM16 gene helped turn the cells into brown fat cells. It may be possible to do the same in people, Spiegelman said.

"You might not have to implant a large amount of engineered precursors in people who are at risk for being obese," Spiegelman said in a statement. One percent might do it, he said.

TIP A METABOLISM

This could potentially tip a person's metabolism in favor of burning off excess calories instead of loading them on as fat. White fat cells do much more than just sit there -- they produce hormones and other compounds that can affect health and make a person even more obese.

Spiegelman's team said their next step is to rev up the PRDM16 control in mice and then see if the mice stay slender even when overfed.

In a second study in the same journal, a Japanese team found that a compound called adiponectin, produced by white fat, works on the brain and helps stimulate the appetites of mice.

Takashi Kadowaki of the University of Tokyo and colleagues said they may have discovered how adiponectin works with another hormone called leptin, also linked to appetite and obesity.

"The fundamental roles of leptin and adiponectin seem to be to preserve an adequate fat reserve: leptin acts as a satiety signal, and adiponectin acts as a starvation signal," Kadowaki said.

They found that adiponectin caused the metabolism of mice to slow down and that levels of the hormone rose during fasting and fell after feeding.

Mice that were deficient in adiponectin ate less and expended more energy, they said. Now the question is whether this mechanism can be manipulated in people, they said.