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We found previously that dietary soy protein, compared with casein, reduced plasma LDL cholesterol and increased HDL cholesterol concentrations in healthy women and men. However, there was considerable variation among individuals. The aim of this study was to characterize the lipoprotein responsiveness of individuals to examine whether different response patterns could be identified. Nine normolipemic men consumed 2 liquid-formula diets of identical composition except that the protein component was either soy protein or casein. After 1 mo of consuming each diet, the subjects’ plasma HDL cholesterol (P < 0.01) and apolipoprotein (apo) A-I (P < 0.05) concentrations were increased by the soy protein diet whereas the ratio of LDL cholesterol to HDL cholesterol was decreased (P < 0.01); total cholesterol, triacylglycerol, LDL cholesterol, apo B and apo A-II were insignificantly affected. In 5 individuals, however, soy protein reduced mean LDL cholesterol, LDL2 cholesterol, and LDL2 apo B concentrations by 26% and plasma apo B by 16%, whereas HDL cholesterol increased by 11% . In 3 other individuals, soy protein increased mean HDL cholesterol by 17% and plasma apo A-I by 12%, but did not lower LDL. In 1 subject, soy protein decreased LDL2 cholesterol by 11% and increased plasma triacylglycerol by 40%, but neither HDL cholesterol nor apo A-I increased. We identified 3 types of lipemic responses to dietary soy protein involving a reduction in atherogenic LDL and increase in antiatherogenic HDL. In most subjects, the effects on both LDL and HDL were favorable, although fewer experienced either an increase in HDL or a decrease in LDL2. [ABSTRACT FROM AUTHOR]

Mutations in apolipoprotein B (APOB) may reduce binding of low density lipoprotein (LDL) to the LDL receptor and cause hypercholesterolemia. We showed that heterozygotes for a new mutation in APOB have hypobetalipoproteinemia, despite a reduced binding of LDL to the LDL receptor. APOB R3480P heterozygotes were identified among 9,255 individuals from the general population and had reduced levels of apoB-containing lipoproteins. Most surprisingly, R3480P LDL bound with lower affinity to the LDL receptor than non-carrier LDL in vitro, and these results were confirmed by turnover studies of LDL in vivo. In very low density lipoprotein (VLDL) turnover studies, the amount of VLDL converted to LDL in R3480P heterozygotes was substantially reduced, suggesting that this was the explanation for the hypobetalipoproteinemia observed in these individuals. Our findings emphasized the importance of combining in vitro studies with both human in vivo and population-based studies, as in vitro studies often have focused on very limited aspects of complex mechanisms taken out of their natural context. [ABSTRACT FROM AUTHOR]