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Fatty acid uptake in normal human myocardium
1Department of Molecular Biophysics, University of Bochum, FRG.
Circulation Research
|September 1, 1991
Summary
A 40-kDa fatty acid binding protein on cardiac endothelial cells facilitates myocardial fatty acid uptake. This process is saturable, indicating a specific transport mechanism rather than simple diffusion.
Area of Science:
- Biochemistry
- Cardiology
- Cell Biology
Background:
- Fatty acid binding protein (FABP) identified in rat aortic endothelial cells.
- A 40-kDa FABP with high affinity for long-chain fatty acids exists in rat heart myocytes.
- Proposed role of endothelial FABP in mediating myocardial fatty acid uptake.
Purpose of the Study:
- To evaluate the hypothesis that endothelial membrane FABP mediates myocardial fatty acid uptake in vivo.
- To investigate the kinetics of fatty acid influx into the myocardium.
Main Methods:
- Scintigraphic techniques used to examine tracer-labeled fatty acid influx in 15 normal subjects.
- Plasma fatty acid concentration and perfusion rates modulated via nutrition and exercise.
- Functional relations developed to analyze fatty acid transport, considering unstirred layers.
Main Results:
- Myocardial fatty acid influx rate is saturable with increasing plasma fatty acid concentration and plasma flow.
- Data suggest fatty acid influx occurs at the capillary surface, not in extravascular space or unstirred layers.
- Saturable influx characterized by Michaelis-Menten parameters: Km (0.24 ± 0.024 μmol/g) and Vmax (0.37 ± 0.013 μmol/g·min).
Conclusions:
- Myocardial fatty acid influx is a saturable, non-diffusional process.
- Findings support the role of the 40-kDa cardiac endothelial FABP in mediating fatty acid uptake.
- The interaction of fatty acids with endothelial FABP is the initial step in myocardial uptake.