Grant: CIHR Fellowship

Obesity is a well-known risk factor for chronic diseases, including type 2 diabetes and heart disease. Despite intensive research, there are no treatments that effectively promote weight loss for long periods of time. At the center of obesity is the fat cell. Surprisingly, no treatments specifically target fat cells, which need a complicated roadmap of signals to grow. One protein that provides direction for these signals is 14-3-3zeta, which we previously found to have important roles in the growth of fat cells. Depending on conditions, proteins that interact with 14-3-3zeta can change. For example, during fat cell growth, a large number of proteins that associate with 14-3-3zeta are those that influence RNA splicing. When RNA splicing is inhibited, fat cells do not develop properly. Recently, high-fat diet-induced obesity has been found to alter RNA splicing in fat cells. This raises the question of whether obesity causes the aberrant recruitment of 14-3-3zeta-associated RNA splicing factors, thereby promoting the development of obesity. Therefore, in my post-doctoral fellowship, I wish to undertake new studies aimed at testing whether altered RNA splicing promotes the development of obesity and understand in great detail how 14-3-3zeta controls this process in fat cells. Results from these studies will determine whether 14-3-3zeta can influence the development of obesity, and they may lead to new ways to prevent or treat obesity, a disease that affects people of all ages and throughout the world.