Aspects of fatty acid metabolism in vascular endothelial cells.
Long-chain fatty acids are an important source of energy in vascular endothelium. Their oxidation is stimulated by carnitine and inhibited by blockage of the mitochondrial respiratory chain. Excess fatty acid can be reversibly stored as triacylglycerol in the cells. Cultured vascular endothelial cells, in contrast to cardiac vascular endothelium in the intact heart, take up and intracellularly degrade artificial chylomicrons (intralipid enriched with apolipoprotein C-II) but not natural chylomicrons. Fatty acids not bound to albumin, such as those generated from chylomicrons in the lipoprotein lipase reaction, although initially a good source of substrate for beta-oxidation, endanger heart function. Fatty acid excess initiates the breakdown of the endothelial barrier between the vascular lumen and interstitium; it may precipitate edema formation, lead to insufficient oxygenation and finally cause loss of heart function.
D002331:Carnitine / Q000378:metabolism / Q000494:pharmacology; D002463:Cell Membrane Permeability / Q000187:drug effects; D002478:Cells, Cultured; D002914:Chylomicrons / Q000378:metabolism; D003331:Coronary Vessels / Q000378:metabolism; D004487:Edema / Q000139:chemically induced; D004730:Endothelium, Vascular / Q000378:metabolism*; D004734:Energy Metabolism; D005227:Fatty Acids / Q000378:metabolism* / Q000494:pharmacology; D006801:Humans; D008071:Lipoprotein Lipase / Q000378:metabolism; D010084:Oxidation-Reduction; D010085:Oxidative Phosphorylation; D010587:Phagocytosis; D010873:Pinocytosis; D014280:Triglycerides / Q000378:metabolism; D014469:Umbilical Arteries / Q000378:metabolism
D002914:Chylomicrons; D005227:Fatty Acids; D014280:Triglycerides; D008071:Lipoprotein Lipase; D002331:Carnitine