A heart that has become enlarged in response to a pressure overload, such as with high blood pressure, has reduced function compared to a normal heart. This impaired function is particularly apparent during and after interruption of the blood supply, which can occur when a blood clot blocks a diseased coronary artery, or during open heart surgery. This reduced heart function can be very dangerous for the patient. Enlarged hearts use glucose to a greater extent than normal, a situation that appears to contribute to their exaggerated dysfunction. The mechanisms responsible for the accelerated utilization of glucose in enlarged hearts are not yet known. Dr. Minnie Dai was previously funded by MSFHR for her doctoral training. Currently, she is working to determine the mechanisms behind accelerated rates of glucose utilization in enlarged hearts. Using molecular biology techniques, she will selectively and specifically alter the activity of potentially relevant proteins in order to determine their role in causing accelerated glucose utilization. Her studies are unique in that the activity of proteins will be altered at specific times and will be altered only in the heart – ensuring that changes observed are truly related to alterations in these proteins. Many people suffer ill health because of an enlarged heart. By understanding the mechanisms responsible for their accelerated use of glucose, researchers may be able to identify targets for the development of drugs designed to altered glucose use by enlarged hearts, thereby improving their function.