Uptake and transport of lipid substrates in the heart.
Between 1955-1960 it was realized that the fatty acids circulating in the blood, after transport into the cardiac cells, then beta-oxidation in the myocyte mitochondria, were the major source of energy behind the impressive hydraulic performance of the heart. Only albumin-bound fatty acids and, to a lesser extent, cholesterol ester and triglyceride fatty acids have access to the cardiac cells. Circulating phospholipid fatty acids are excluded. From experiments with isolated perfused hearts it was concluded that fatty acid uptake by the myocardium was essentially an energy independent process. An important question still pending in the literature concerns the mechanisms of fatty acid transport through the capillary endothelium, through the cardiac cell plasma membrane and then through the intracellular compartments. The most plausible model now emerging considers that specific fatty acid-binding proteins, sequentially disposed along this cascade of barriers, might facilitate and drive the flux of fatty acids entering the cardiac cells.
Fournier
N C
NC
Nestlé Research Department, Nestec Ltd., Vevey, Switzerland.
D000818:Animals; D001693:Biological Transport, Active; D002196:Capillaries / Q000378:metabolism; D002788:Cholesterol Esters / Q000378:metabolism; D005227:Fatty Acids / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D050356:Lipid Metabolism; D009206:Myocardium / Q000378:metabolism*; D010743:Phospholipids / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism
D002788:Cholesterol Esters; D005227:Fatty Acids; D005230:Fatty Acids, Nonesterified; D010743:Phospholipids; D014280:Triglycerides