A research team at the Okinawa Institute of Science and Technology developed a mouse model unable to produce a specific protein designated XRN1 associated with appetite regulation.  Mice unable to synthesize XRN1 were resistant to both insulin and leptin a hormone that suppresses appetite.  Mice unable to express XRN1 also released an appetite stimulating protein AgRP from the hypothalamus.

The gene-deleted mice gained weight after weaning and by 12-weeks of age were obviously obese with a feed intake twice the level of control mice.

Knowledge concerning regulation of appetite, if applicable to other species could indicate approaches to modifying appetite to prevent obesity in genetically predisposed individuals.