Inhibition of lipoprotein lipase with tetrahydrolipstatin or its dissociation with heparin reduced cardiac uptake of triglycerides by 82% and 64%, respectively (P < 0.01).
The heart effectively removes circulating triglycerides and core lipids primarily through LPL hydrolysis rather than its bridging function.
p-value: p=< 0.01
Long-chain fatty acids (FA) supply 70-80% of the energy needs for normal cardiac muscle. To determine the sources of FA that supply the heart, (14)Cpalmitate complexed to bovine serum albumin and (3)Htriolein triglyceride (TG) incorporated into Intralipid were simultaneously injected into fasted male C57BL/6 mice. The ratio of TG to FA uptake was much greater for hearts than livers. Using double-labeled Intralipid with (3)Hcholesteryl oleoyl ether (CE) and (14)CTG, we observed that hearts also internalize intact core lipid. Inhibition of lipoprotein lipase (LPL) with tetrahydrolipstatin or dissociation of LPL from the heart with heparin reduced cardiac uptake of TG by 82 and 64%, respectively (P < 0.01). Palmitate uptake by the heart was not changed by either treatment. Uptake of TG was 88% less in hearts from LPL knockout mice that were rescued via LPL expression in the liver. Our data suggest that the heart is especially effective in removal of circulating TG and core lipids and that this is due to LPL hydrolysis and not its bridging function.
Augustus et al. (2003) studied Normal cardiac muscle metabolism. Inhibition of lipoprotein lipase (LPL) with tetrahydrolipstatin or dissociation with heparin vs. Control/baseline was evaluated on Cardiac uptake of triglycerides (p=< 0.01). Inhibition of lipoprotein lipase with tetrahydrolipstatin or its dissociation with heparin reduced cardiac uptake of triglycerides by 82% and 64%, respectively (P < 0.01).
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