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pubmed:abstractText |
In many individuals, LDL-cholesterol levels rise following increased consumption of dietary cholesterol or saturated and trans-monounsaturated fatty acids. In others, a reduction of cholesterogenesis fully compensates for these effects. In responding individuals, much of the increase in LDL-cholesterol observed may result directly from an increase in plasma cholesteryl ester transfer protein activity whose effect is not mediated by hepatic LDL receptors.
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