The study showed how a protein called SH2B1 can regulate body weight, the use of energy, or the action of leptin and insulin. It may also moderate the effect of a high-fat diet on weight balance.

An earlier study by the same team had showed that mice with a lack of SH2B1 become diabetic, obese, or even unable to stop eating because their brains lost the ability to sense signals from leptin and insulin that indicate when to stop the food intake. The experiments included different types of mice: some that were normal, some genetically altered so they have SH2B1 only in the brain, and mice that didn`t had the gene responsible for SH2B1.

The study showed that restoring the level of SH2B1 in the brain lead to a re-establishment of metabolic disorders in case of mice with a lack of SH2B1 and also improved the brain`s ability to respond to leptin signals. The mice that were modified so they could produce extra SH2B1 responded to leptin signals and didn`t become obese even if they were on a high-fat diet.

SH2B1 seems to have a regulatory role in the system that is processing leptin and insulin signals, according to researcher Liangyou Rui. The imbalance between energy intake and energy use leads to obesity, but it may be caused by alterations of leptin and insulin signals, says Rui.