Torrey Pines Institute for Molecular Studies science image
Torrey Pines Institute for
Molecular Studies

3550 General Atomics Court, 2-129
San Diego, CA 92121-1122
USA

Torrey Pines Institute for
Molecular Studies

5775 N. Old Dixie Highway
Fort Pierce, FL 34946-7302
USA

About TPIMS
Heart Disease
Free fatty acids (FFA) are the major source of energy for the heart. Normal cardiac function therefore requires an adequate and constant supply of FFA, which is obtained from the blood that supplies the heart. The heart must efficiently transport the FFA from the blood, across the heart cell membranes and into the cytoplasm where the FFA can be used for the energy needed to drive heart muscle.

Kleinfeld, Carley and Kampf's laboratory uses the novel techniques, akin to the ones untilized with type II diabetes research, to investigate how FFA are transported across the heart cell membranes. To do this, their laboratory has isolated individual heart cells, microinjected these cells with a fluorescent indicator of FFA and used quantitative fluorescent microscopy to monitor FFA transport in living heart cells. The results that are obtained are similar to those in adipocytes, suggesting that heart cells have mechanisms for taking up as well as releasing FFA.

Although the heart requires sufficient quantities of FFA for normal function, too much FFA may be deleterious. In collaboration with FFA Sciences, Dr. Kleinfeld's lab has developed fluorescent indicators that can specifically detect the portion of FFA in blood that is soluble in the water phase of plasma, the unbound FFA (FFAu). The investigations indicate that in acute cardiovascular disease, blood levels of FFAu may increase as much as 100 fold above normal. FFAu elevations occur very early in acute cardiac events (ischemia) and may therefore provide an early indicator of a heart attack. Moreover, the lab's studies of heart attack patients demonstrate that elevated FFAu levels at the earliest times are prognostic for immediate (hours to days) risk of death. These studies raise the possibility that the FFAu themselves may mediate the deleterious effects and suggest that therapies that rapidly lower FFAu levels might reduce deaths due to myocardial infarctions.

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