Effect of changing dietary fat saturation on low-density lipoprotein metabolism in man. 1981

J D Turner, and N A Le, and W V Brown

The mechanism of change in low-density lipoprotein (LDL) levels by diets differing in fat saturation have been studied. Turnover of 125I-LDL was measured in eight subjects with type II hyperlipoproteinemia and in seven normal control subjects during two dietary periods containing 40% of calories as either safflower oil (polyunsaturated fat, PSF) or as lard (saturated fat, SF). Higher levels of LDL apoprotein and LDL-cholesterol were observed in both groups on saturated fat. Subjects with elevated LDL levels (type II) showed a more marked effect of polyunsaturated fat with 25% lower LDL production rate as compared to a reduction of only 10% for the control group. On the PSF diet, the production rate in type II (12.7 mg.kg-1.day-1) was not statistically different from normal subjects (10.5 mg.kg-1.day-1). On this diet, the higher levels of LDL cholesterol in the type II subjects (as compared to controls) were due to a lower fractional clearance rate, mean of 0.27/day compared to a mean of 0.39/day for the normal subjects. Although individuals with type II hyperlipoproteinemia may have a primary clearance defect, the major reduction in plasma cholesterol concentrations achieved with a diet high in polyunsaturated fat can be attributed to a significantly lower LDL production.

UI MeSH Term Description Entries
D006951 Hyperlipoproteinemias Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation. Hyperlipoproteinemia
D008075 Lipoproteins, HDL A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases. High Density Lipoprotein,High-Density Lipoprotein,High-Density Lipoproteins,alpha-Lipoprotein,alpha-Lipoproteins,Heavy Lipoproteins,alpha-1 Lipoprotein,Density Lipoprotein, High,HDL Lipoproteins,High Density Lipoproteins,Lipoprotein, High Density,Lipoprotein, High-Density,Lipoproteins, Heavy,Lipoproteins, High-Density,alpha Lipoprotein,alpha Lipoproteins
D008077 Lipoproteins, LDL A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues. Low-Density Lipoprotein,Low-Density Lipoproteins,beta-Lipoprotein,beta-Lipoproteins,LDL(1),LDL(2),LDL-1,LDL-2,LDL1,LDL2,Low-Density Lipoprotein 1,Low-Density Lipoprotein 2,LDL Lipoproteins,Lipoprotein, Low-Density,Lipoproteins, Low-Density,Low Density Lipoprotein,Low Density Lipoprotein 1,Low Density Lipoprotein 2,Low Density Lipoproteins,beta Lipoprotein,beta Lipoproteins
D008078 Cholesterol, LDL Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol. LDL Cholesterol,Cholesteryl Linoleate, LDL,LDL Cholesteryl Linoleate,Low Density Lipoprotein Cholesterol,beta-Lipoprotein Cholesterol,Cholesterol, beta-Lipoprotein,beta Lipoprotein Cholesterol
D008079 Lipoproteins, VLDL A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues. Pre-beta-Lipoprotein,Prebeta-Lipoprotein,Prebeta-Lipoproteins,Very Low Density Lipoprotein,Very-Low-Density Lipoprotein,Very-Low-Density Lipoproteins,Lipoprotein VLDL II,Lipoproteins, VLDL I,Lipoproteins, VLDL III,Lipoproteins, VLDL1,Lipoproteins, VLDL2,Lipoproteins, VLDL3,Pre-beta-Lipoproteins,Lipoprotein, Very-Low-Density,Lipoproteins, Very-Low-Density,Pre beta Lipoprotein,Pre beta Lipoproteins,Prebeta Lipoprotein,Prebeta Lipoproteins,VLDL Lipoproteins,VLDL1 Lipoproteins,VLDL2 Lipoproteins,VLDL3 Lipoproteins,Very Low Density Lipoproteins
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D010641 Phenotype The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment. Phenotypes
D012016 Reference Values The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality. Normal Range,Normal Values,Reference Ranges,Normal Ranges,Normal Value,Range, Normal,Range, Reference,Ranges, Normal,Ranges, Reference,Reference Range,Reference Value,Value, Normal,Value, Reference,Values, Normal,Values, Reference
D002784 Cholesterol The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. Epicholesterol

Related Publications

J D Turner, and N A Le, and W V Brown
May 1997, The American journal of clinical nutrition,
J D Turner, and N A Le, and W V Brown
March 1987, The Journal of clinical investigation,
J D Turner, and N A Le, and W V Brown
January 1992, Journal of lipid research,
J D Turner, and N A Le, and W V Brown
June 1995, Journal of lipid research,
J D Turner, and N A Le, and W V Brown
December 1997, The Journal of clinical endocrinology and metabolism,
J D Turner, and N A Le, and W V Brown
May 2004, Family medicine,
Copied contents to your clipboard!