The findings also suggest that certain variants of SH2-B may underlie obesity in humans.
The researchers found that SH2-B keeps the brain sensitive to the fat hormone leptin, which is produced by fat tissue and sends signals to the brain concerning body fat levels. In response to those signals, the brain makes adjustments to appetite and energy expenditure in order to maintain a more normal body weight.
Mice that lacked SH2-B overate and became obese, the study found. These mice also developed a metabolic syndrome featuring high blood concentrations of leptin, insulin and lipids (fats). The mice also developed fatty livers and high blood sugar.
The study appears in the August issue of the journal Cell Metabolism.
"Our findings reveal SH2-B as an important positive regulator of leptin sensitivity inside cells of the brain region known as the hypothalamus," study senior author Liangyou Rui, of the University of Michigan Medical School, explained in a prepared statement. The hypothalamus integrates hormonal, neuronal and nutrient-related signals to maintain body weight.
"Because SH2-B sensitizes both leptin and insulin, action drugs that mimic or enhance SH2-B action may improve insulin and leptin sensitivity and have potential value in treatment of obesity and type 2 diabetes," Rui said.