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By Rodolfo Paoletti; David Kritchevsky

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Extra info for Advances in lipid research. Volume 11

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H. on ordinary diet. a R,ecalculated from data given by Sardet ct al. (1972a). C More recently, work in other laboratolies has confirn1ed and significantly extended Switzer's observations and in addition provided a basis for comparing the abnormal LDL in cholestasis with those in familial LCAT deficiency. Picard and Veissiere (1970a) showed that the LDL of patients with cholestasis yield several subfractions upon being filtered through 2'% agarose gel and that a major subfraction of abnorn1ally large molecular size (peak II, Fig.

The sn1aller n10lecular weight VLDL and LDL also are probably generated by the action of lipoprotein lipase on chylon1icrons and larger VLDL. Their abnormal composition is consistent with the possibility that LCAT normally decreases the unesterified cholesterol, lecithin, and triglyceride of VLDL and LDL by promoting nonenzyn1atic transfers of HDL cholesteryl ester to the VLDL and LDL. Finally, the data suggest that smaller molecular weight HDL also are related to chylomicrons and raise the possibility that apo-A proteins derived from the surfaces of chylomicrons act with LCAT to forn1 HDL cholesteryl ester and dispose of chylon1icron polar lipid.

Negatively stained with phosphotungstic acid; approx. 189,000 X. B, small molecular weight HDL of patient A. ; approx. 231,000 X. From Forte et al. (1971a); see also Torsvik et al. (1970). 19 Lecithin: Cholesterol Acyltransferase 20 Flotation rate (F 1. 20 ) 10 o 3 , ,n : :i I. I: \ :; \\ ,/ I ~ \: ,: - - A. A. A. :. FIG. 11. Analytical ultracentrifugation of HDL subfractions from a patient with familial LeAT deRciency. Large and small n10lecular weight subfractions from patient A. A. (see also Fig.

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