By Rodolfo Paoletti; David Kritchevsky
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Additional resources for Advances in lipid research. Volume 11
This apparently contradictory finding should be checked by other investigators, especially in view of the report by Torsvik (1969) that appreciable an10unts of n1aterial that reacts with con1mercial antisera to HDL are present in lipoprotein fractions other than HDL in the plasma of patients with familial LCAT deficiency. Comparison of the abnorn1alities in cholestasis with those in fan1ilial LCAT deficiency is complicated not only by the relative lack of inforn1ation regarqing the VLDL and HDL, but also by the variable liver dan1age usually present.
R. were subfractionated by filtration through 2% agarose gel columns (see Figs. 3-5). 063 grn/ml. 25 gm/ml had previously been heat-inactivated. 063 gm/ml were reisolated by preparative ultracentrifugation. of unesterified cholesterol and lecithin to HDL. 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.
1973b) have been performed on four of the Norwegian patients with striking results. In these patients, isocaloric, low fat (approximately 6% of calories from fat) or fat-free (less than 1'% of calories from fat) diets decreased plasma triglycerides and cholesterol (Table VIII), whereas subsequent hypercaloric, high carbohydrate diets or isocaloric diets in which the fat was provided by medium chain triglyceride increased the concentration of plasma triglyceride toward its starting value without affecting the concentration of cholesterol.
Advances in lipid research. Volume 11 by Rodolfo Paoletti; David Kritchevsky