Plasma free fatty acids (FFA) are thought to be a major source of lipid fuel for the myocardium. Although the heart contains lipoprotein lipase (LPL), virtually no information is available regarding the possible uptake of triglycerides (TGs, carried by circulating TG-rich lipoproteins) by this tissue in humans. Animal studies have suggested that TGs may supply more fatty acids to the heart than FFA and that TG fatty acid uptake may be increased in hypertriglyceridemia. We studied postabsorptive non-diabetic adults (N = 6) during diagnostic coronary angiography. Beginning 90 minutes before the procedure and continuing until blood sampling was complete, [1-14 C]oleate and a lipid emulsion labeled with [9,10-3H]triolein were infused in tracer amounts. Paired arterial (A) and coronary sinus (CS) samples were taken every 4 min for 20 min. Systemic and myocardial kinetics, including the production of [3 H]oleate generated by the action of LPL on the infused TG tracer, were determined. Fractional spillover of LPL-generated fatty acids was calculated as the rate of appearance (Ra) of [3 H]oleate divided by the disappearance rate of the [3 H]TG tracer, both for whole body and for the myocardium. Plasma glucose concentrations were lower in CS than in A (85 ± 5 vs 90 ± 4 mg/dL, p < .05). Plasma total FFA concentrations were lower in CS than A (507 ± 119 vs 653 ± 106 μmol/L, p < .001). [14 C]Oleate specific activity (SA) was lower in CS than in A (1.20 ± 0.17 vs 1.34 ± 0.18 dpm/nmol, p < .05), whereas there was no difference in [3 H]oleate SA (4.85 ± 0.97 vs 4.61 ± .96 dpm/nmol, p = .17). Systemic oleate Ra was 2.7 ± 0.6 μmol•kg-1•min-1. Myocardial production of oleate (presumably derived from lipolysis in epicardial adipose tissue) was 0.5 ± 0.1% of systemic Ra. The fractional myocardial extraction of radiolabeled oleate was higher than that of radiolabeled TG (34 ± 5% vs 11 ± 3%, p < .001). The contribution of the heart to whole body disappearance of FFA and TG was 3.1 ± 1.1% and 2.1 ± 0.7%, respectively. Systemic fractional spillover of LPL-generated fatty acids was higher than myocardial (49 ± 7% vs 20 ± 3%, p < .02). These results indicate that in humans, myocardial LPL acts on circulating lipoproteins, resulting in uptake of fatty acids from lipoprotein TG. The heart is a minor site of uptake for both FFA and TGs from a systemic point of view. It is also a minor source of systemic FFA Ra. Myocardial uptake of LPL-generated TG fatty acids is relatively efficient compared with whole body uptake. Additional study is needed to determine whether myocardial TG uptake is increased in individuals with hypertriglyceridemia and whether it increases after ingestion of meals containing fat.
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