Abstract
Long chain fatty acids (LCFAs) provide 70-80% of the energy for cardiac contractile activity. LCFAs are also essential for many other cellular functions, such as transcriptional regulation of proteins involved in lipid metabolism, modulation of intracellular signalling pathways, and as substrates for membrane constituents. When LCFA uptake exceeds the capacity for their cardiac utilization, the intracellular lipids accumulate and are thought to contribute to contractile dysfunction, arrhythmias, cardiac myocyte apoptosis and congestive heart failure. Moreover, increased cardiac myocyte triacylglycerol, diacylglycerol and ceramide depots are cardinal features associated with obesity and type 2 diabetes. In recent years considerable evidence has accumulated to suggest that, the rate of entry of long chain fatty acids (LCFAs) into the cardiac myocyte is a key factor contributing to a) regulating cardiac LCFA metabolism and b) lipotoxicity in the obese and diabetic heart. In the present review we i) examine the evidence indicating that LCFA transport into the heart involves a protein-mediated mechanism, ii) discuss the proteins involved in this process, including FAT/CD36, FABPpm and FATP1, iii) discuss the mechanisms involved in regulating LCFA transport by some of these proteins (including signaling pathways), as well as iv) the possible interactions of these proteins in regulating LCFA transport into the heart. In addition, v) we discuss how LCFA transport and transporters are altered in the obese/diabetic heart.
Highlights
Long chain fatty acids (LCFAs) provide 70-80% of the energy for cardiac contractile activity [1,2]
By regulating the rate of the entry of LCFAs into the cardiac myocytes, these LCFA transport proteins may serve as a key factor contributing to the regulation of LCFA metabolism in healthy hearts, while in obesity and diabetes these proteins may contribute to the lipotoxicity associated with excess lipid accumulation in the heart
Our work has recently demonstrated that electrical stimulation of quiescent cardiac myocytes activates AMPK, which results in the translocation of fatty acid translocase (FAT)/CD36 to the plasma membrane and a concurrent increase in the rate of LCFA transport [16]
Summary
Long chain fatty acids (LCFAs) provide 70-80% of the energy for cardiac contractile activity [1,2]. Acute insulin exposure (30 min) stimulated the rate of LCFA transport into cardiac myocytes by inducing the translocation of only FAT/CD36, but not FABPpm nor FATP1, from an intracellular membrane compartment to the plasma membrane
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