抄録
To elucidate the beneficial role of polyunsaturated fatty acid (PUFA) in the lipoprotein metabolism, we studied the activation of lipoprotein lipase (LPL) by various molecular species of synthetic phosphatidylcholine. A solution of acetoneether powder of rat epididymal fat pads extracted by NH4OH-NH4Cl buffer was used as the LPL source. Apoprotein of very low density lipoprotein was prepared from the serum of a patient with type IIb hyperlipoproteinemia. The substrate was [14C]triolein emulsified in an arabic gum solution. After incubation of the substrate with emulsions of different synthetic phosphatidylcholines for 60min at 37°C, reaction was started by the addition of enzyme extract. LPL activity was assayed by counting labeled fatty acids liberated within 60min.
In the presence of dipalmitoyl phosphatidylcholine (PC), hardly any LPL was activated, whereas the addition of palmitoyl-linoleoyl PC significantly activated LPL. Furthermore, the addition of dilinoleoyl PC almost doubled the LPL activity. When four synthetic PCs—palmitoyl-stearoyl, palmitoyl-oleoyl, palmitoyl-linoleoyl and palmitoyllinolenoyl PCs—were added to the reaction mixture, the extent of activation of LPL was definitely increased in this order. The effect of two PCs—palmitoyl-linoleoyl and linoleoyl-palmitoyl PCs—was compared. The extent of activation by the former exceeded those by the latter, in all concentrations of PC examined, although small. The mean particle size of artificial substrate emulsion determined by an electron microscopic method was 47.5 and 52.7nm in the presence of palmitoylstearoyl PC and palmitoyl-linoleoyl PC, respectively.
These results indicate that LPL was activated by the addition of PC to the substrate. LPL activation was markedly enhanced as the number of unsaturated acyl chains in the PC molecule or the degree of unsaturation of these acyl chains was increased. It is suggested that the increased proportion of PUFA in plasma PC may accelerate the hydrolysis of ingested triglyceride followed by normalization of postprandial hyperlipidemia.
