Abstract
DIETARY cholesterol increases the plasma level of total and low-density lipoprotein (LDL) cholesterol and accelerates the development of atherosclerosis and its complications, but individual responses to a given change in the dietary cholesterol level vary widely.1 2 3 4 5 6 7 Such responses are reproducible to some extent, suggesting genetic as well as physiologic determinants.8 , 9 Several genetic determinants have been identified in nonhuman primates.10 11 12 13 The homeostatic and regulatory mechanisms that maintain a relatively constant level of plasma cholesterol despite changes in dietary cholesterol intake include alterations in the efficiency of intestinal absorption and in the rates of cholesterol biosynthesis, LDL-receptor activity, secretion of cholesterol into bile, and hepatic conversion of cholesterol into bile acids, the chief metabolic product of cholesterol.5 , 7 , 14 , 15