Effect of dietary cholesterol on postprandial lipoproteins in three phenotypic groups
Author(s) -
Peter Clifton,
PJ Nestel
Publication year - 1996
Publication title -
american journal of clinical nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.608
H-Index - 336
eISSN - 1938-3207
pISSN - 0002-9165
DOI - 10.1093/ajcn/64.3.361
Subject(s) - postprandial , cholesterol , meal , medicine , endocrinology , lipoprotein , chemistry , high density lipoprotein , biology , diabetes mellitus
Dietary cholesterol appears to be associated with long-term cardiovascular risk even after its potential for cholesterol elevation has been accounted for, but the mechanism is unknown. Our aim in this study was to determine the postprandial lipoprotein changes after a high-cholesterol load (equal to about three eggs) eaten with a low-fat meal by three phenotypic groups [normal, high low-density-lipoprotein (LDL)-cholesterol concentration, and high plasma triacylglycerol concentration] and compare them with the changes seen after a low-fat meal without cholesterol. Twenty-one normolipidemic and hyperlipidemic men and women were studied on two occasions after a single meal, one containing 19 g fat and 700 mg cholesterol, the other containing a similar amount of fat but no cholesterol. Their plasma intermediate-density lipoproteins (IDLs), LDLs, and high-density lipoproteins (HDLs) were separated by isopycnic ultracentrifugation. The addition of 700 mg cholesterol to the meal increased the amount of cholesterol and triacylglycerol in the large triacylglycerol-rich lipoproteins (Sf > 1000), particularly in the hypertriacylglycerolemic group (P = 0.02, fat meal compared with fat and cholesterol meal). In the hypertriacylglycerolemic group the normal fall in HDL cholesterol after a fat meal was reduced by 87% (P = 0.02, fat meal compared with fat and cholesterol meal). Both of these changes may be atherogenic. There was no increase in any candidate atherogenic particle (e.g., small very-low-density lipoprotein, IDL, or LDL) with the acute dietary cholesterol load. Thus, dietary cholesterol does not acutely alter postprandial lipoproteins to produce a more atherogenic profile except possibly in hypertriacylglycerolemic subjects.
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