Obesity is a well-known risk factor for diseases, including type 2 diabetes and heart disease. Despite intensive research, current treatments fail to promote significant weight loss or reduce weight for long periods of time. Surprisingly, no treatments specifically target adipocytes, or fat cells. Adipocytes are the primary cells involved in the development of obesity, and they grow through a complicated roadmap of signals that requires precise direction. Proteins of the 14-3-3 family are known as molecular scaffolds and have the ability to direct this type of signal traffic.
We previously found that one member, 14-3-3zeta, has important roles in the growth of fat cells. Mice that were genetically modified to have no 14-3-3zeta in all cells had less fat than normal mice. In contrast, when they were made to have more 14-3-3zeta in every cell, they actually gained more weight when fed foods rich in fat. This raises the question of whether having higher levels of 14-3-3ζ in fat cells can cause obesity.
Therefore, the aims of this proposal are to (1.) understand how 14-3-3zeta controls the growth of a fat cell, (2.) figure out whether it is involved in fat cell function, and (3.) test whether having more 14-3-3zeta causes obesity. Different techniques will be used to research these aims, and the ultimate goal of this proposal is to figure out whether 14-3-3zeta can be targeted in the future for the treatment of obesity, a disease that affects people of all ages and throughout the world.