This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. A central problem in cardiac physiology is to determine the sources of energy production. Many studies have measured oxidation of each exogenous substrate available to the heart and have generally concluded that long chain fatty acids are the preferred substrate for oxidation, contributing 60-70% of acetyl-CoA production under physiological conditions. The remainder of energy production depends on the concentration of alternative substrates and neurohumoral conditions. However, a basic difficulty in understanding cardiac metabolism of fatty acids is that the endogenous triglyceride pool may also contribute to energy production. Triglyceride content is abnormal in ischemic, diabetic and hypertrophied hearts, yet until recently triglycerides were thought to function as relatively inert stores of long chain fatty acids with little role in either normal physiology or disease. There is now increasing interest in the possibility that intramyocellular triglycerides play a central role in the pathogenesis of impaired left ventricular function among patients with type 2 diabetes via stimulation of apoptosis. However, almost nothing is known about the kinetics of triglyceride turnover and the extent to which exogenous long chain fatty acids exchange with triglyceride stores while simultaneously serving as a critical source for energy production.
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