出版社：American Society for Biochemistry and Molecular Biology
摘要：The role of lipoprotein lipase (LPL) in the generation of low density lipoprotein (LDL) and high density lipoprotein (HDL) was investigated. Intravenous injections of high titer goat antiserum against highly purified chicken LPL into fasted roosters quantitatively blocks the removal of plasma VLDL triglyceride (1976. J. Lipid Res. 17: 498-505). Analyses of the chemical components of lipoproteins after 8 hr of LPL inhibition showed that the very low density lipoprotein (VLDL) concentration increased over 10-fold, while LDL and HDL concentrations decreased by 5-fold and 48%, respectively. LDL and HDL cholesterol levels decreased logarithmically over the 8-hr period, with half-lives of 2.4 and 6 hr, respectively. The composition of these lipoprotein fractions on a percent weight basis changed significantly. Experimental LDL contained 37% less phospholipid, 64% less cholesterol, and 2.3-fold more triglyceride than control LDL. Experimental HDL contained 3.1-fold more triglyceride and 50% less unesterified cholesterol than control HDL. The Stokes' radii of HDL were determined by gel filtration on Biogel A5M and Ultrogel AcA 22: the radius of experimental HDL (44.9 A) was smaller than that of control HDL (55.4 A). These measurements were confirmed by electron microscopy (43 and 54 A, respectively). After rate zonal ultracentrifugations of plasma samples, control LDL was clearly resolved, while no LDL could be detected in the experimental samples. Rate zonal ultracentrifugations of plasma samples also indicated that control HDL had a higher flotation rate than experimental HDL. Equilibrium zonal ultracentrifugation showed experimental HDL to be more dense than control HDL with hydrated densities of 1.118 and 1.113 g/ml, respectively. These experiments provide in vivo evidence that LDL is a direct metabolic product of VLDL and that LPL plays a role in the transfer of surface constituents from VLDL to HDL.-Behr, S. R., J. R. Patsch, T. Forte, and A. Bensadoun. Plasma lipoprotein changes resulting from immunologically blocked lipolysis.
