Scientists long ago identified the appetite-suppressing hormone Leptin and the way it works on the brain to control hunger. Now there is more evidence that the tendency to obesity and perhaps the development of diabetes, may have links to the brain.

In studies, mice who were lacking in the protein SH2B1 were obese and developed diabetes. Replacing the SH2B1 in mice lacking this protein prevented obesity and the mice did not develop diabetes. It even prevented obesity in mice being fed a high-fat diet, which indicates that SH2B1 in the brain is necessary to regulate body weight and fat content.

According to the study published in the Journal of Clinical Investigation, neuronal SH2B1 regulates energy and glucose metabolism at least in part by enhancing leptin sensitivity in the brain, particularly in the hypothalamus. Systemic deletion of SH2B1 resulted in severe leptin resistance. Leptin resistance precedes the onset of obesity in mice lacking SH2B1. Restoration of SH2B1 in mice corrected leptin resistance.

Source: Journal of Clinical Investigation