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L L Rudel

Publications and source records attributed to L L Rudel.

131 records · Page 8Linked to original sources

Age and dietary polyunsaturated fat alter high density lipoprotein subfraction cholesterol concentrations in a pediatric population of African green monkeys.

African green monkeys were raised from birth to 60 months of age on diets containing cholesterol (0.8 mg/kcal) and enriched in polyunsaturated (polyunsaturated to saturated fat ratio [P:S] = 2.5) or saturated (P:S = 0.3) fat. Lipoproteins were isolated from plasma of a group of animals (N = 123) and were separated by gel filtration chromatography at 9, 14, 26, 38, and 50 months of age, which covered a period through adolescence into young adulthood. Total plasma cholesterol (TPC) concentrations were 16% lower (p = 0.01) in the polyunsaturated fat-fed group, and high density lipoprotein (HDL) cholesterol concentrations averaged 20% lower (p = 0.008) in this group between 14 and 50 months of age, while plasma apolipoprotein A-I (apo A-I) averaged 7% lower (p = 0.06) over this age interval in the animals. The HDL cholesterol to apo A-I ratio was found to be significantly lower (p = 0.006) in the animals fed the polyunsaturated fat diet. This suggested that the HDL subfraction distribution might differ between groups. In a subset of animals (n = 105, 64 male and 41 female), HDL was subfractionated by density gradient ultracentrifugation into six subfractions, HDL-I to HDL-VI, from lowest to highest density. The saturated fat-fed animals had significantly higher cholesterol concentrations in HDL-I and significantly lower cholesterol concentrations in HDL-III, HDL-IV, and HDL-V. These effects held across all ages studied; therefore, these diet effects were not age dependent. In both diet groups, the HDL subfraction pattern changed with age such that the HDL-I and HDL-II cholesterol concentrations decreased, and those of HDL-IV, HDL-V, and HDL-VI increased as the animals matured. The decrease in HDL-I with age appeared to result primarily from a decrease in HDL-I in males, while the HDL-I cholesterol concentration in females did not change with age. We conclude that diet, age, and gender all affect HDL subfraction distribution and therefore can potentially modify the relative atherogenicity of the plasma HDL populations. It remains for future studies to demonstrate the effectiveness of each subfraction in promoting or preventing the cholesterol deposition of atherosclerosis.

Aging↗

Atherogenic diet-induced modification of the subfraction distribution of high density lipoproteins in monkeys.

High density lipoproteins (HDL) were isolated from the plasma of adult male African green monkeys fed control or atherogenic diets and were then subfractionated in a density gradient by centrifugation at 50,000 rpm, 20 degrees C for 18 hours in the Beckman VTi50 vertical rotor. Material from the gradient was pooled into six subfractions for further analysis. With increasing density across the gradient, the subfractions had progressively decreasing flotation rates, molecular weights, apo A-I/apo A-II mass ratios, lipid percentages of mass, and average sizes. Apoprotein content per particle was reasonably constant compared to lipid content. The physical and chemical properties of the HDL subfractions suggested that the gradient separated three subclasses of HDL equivalent to HDL 2b, HDL 2a, and HDL3 of human beings. When values among animals were compared, the atherogenic diet shifted the relationship between total plasma cholesterol concentration and total HDL concentration from a positive to a negative correlation. The subfractions most affected were those of d less than 1.10 g/ml (HDL2b), while the 1.10 less than d less than 1.13 g/ml (HDL2a) subfractions were affected to a lesser degree; the more responsive the animal to dietary cholesterol, the lower was the mass concentrations of these subfractions. This pattern suggested that diet-induced changes in HDL2 subfraction particle concentrations may be related to the development of atherosclerosis in African green monkeys; parallel changes in particle composition were not identified.

Animals↗

Effects of saturated and polyunsaturated dietary fat on the concentrations of HDL subpopulations in African green monkeys.

The effect of the type of dietary fat on the concentrations and compositions of high density lipoprotein (HDL) subpopulations was studied in groups of African green monkeys consuming 40% of calories as fat supplied as saturated fat (P/S = 0.3) or polyunsaturated fat (P/S = 2.2) in the presence of either 0.8 mg or 0.03 mg cholesterol/kcal. Plasma HDL cholesterol concentrations were lower in polyunsaturated fat-fed animals. The distribution of mass among HDL subfractions was assessed by analytic ultracentrifugation (AnUC), density gradient ultracentrifugation (DGUC), and polyacrylamide gradient gel electrophoresis (GGE). This made it possible to characterize and quantitate the HDL subpopulations HDL2b, HDL2a, HDL3a, HDL3b, and HDL3c (arranged in order of decreasing particle size and decreasing cholesterol content). Polyunsaturated fat-fed animals had lower concentrations of the large, cholesterol-rich HDL2b subpopulation, as well as higher concentrations of intermediate size HDL (HDL2a and HDL3a on the high cholesterol diet; HDL3a and HDL3b on the low cholesterol diet). Consistent with the observed fat-related redistribution of HDL mass, the saturated fat-fed monkeys had higher apo A-I/apo A-II ratios. The larger HDL often contained detectable apo E; however, the concentration of apo E in HDL was low in both saturated and polyunsaturated fat-fed animals. Thus, compared to saturated fat, dietary polyunsaturated fat induced the formation of smaller size HDL subpopulations and, therefore, an overall lower cholesterol content per particle for plasma HDL.

Animals↗

Increased circulating levels of an endogenous digoxin-like factor in hypertensive monkeys.

An endogenous, immunoreactive digoxin-like factor (endoxin) was measured in the plasma of nonhuman primates with hypertension. Both normotensive and hypertensive rhesus monkeys had levels of endoxin that significantly correlated with their systolic or diastolic blood pressure. Vervet monkeys with experimentally produced chronic Goldblatt hypertension had significantly elevated endoxin, but not plasma renin. These data suggest that increased plasma endoxin may be a contributing factor in the development of hypertension.

Animals↗