Grant: Project Grant

In Canada, there is a growing number of people who develop a condition called heart failure. Simply stated, clinical heart failure is a condition that is defined by poor heart function that prevents the heart from pumping enough blood to the rest of the body for proper organ function. As a result, heart failure patients have a very poor quality of life. Although heart failure is often a "chronic" condition, the chances of dying at one year following diagnosis are between 20-30%, even with our most state-of-the-art treatments. Due to the short life expectancy and poor quality of life of the heart failure patient, the increasing amount of people developing heart failure is a major medical concern. In fact, the lifetime risk of developing heart failure for North American adults who have reached 45 years of age is 20%. As such, there is the need for new strategies to treat this debilitating condition and improve the health of these heart failure patients. My lab has been investigating the non-conventional mechanisms that contribute to heart failure (i.e. the contribution of other organs to poor health outcomes in heart failure patients). Recently, we have generated exciting data that indicates that heart failure induces abnormal cellular processes in fat cells that then causes cardiac insulin resistance (essentially the heart becomes resistant to the effects of insulin and cannot extract sugar from the blood to subsequently use as a fuel for energy). This implicates communication between organs (i.e. heart and fat) that can lead to the worsening health of people with heart failure. As such, the objective of this project is to test whether or not heart failure-induced changes in fat cells contribute to worsening heart failure and understand the mechanisms by which this occurs. We will use mice with heart failure as our model in order to better understand how abnormal cellular processes in fat cells communicate with the heart to cause worsening heart function.