Dietary palmitic acid raises plasma LDL cholesterol relative to oleic acid only at a high intake of cholesterol.
Using a crossover design, the effects of exchanging up to 10% dietary energy (%en) between oleic (18:1) and palmitic acid (16:0) on plasma lipoprotein metabolism was investigated in 12 normocholesterolemic cebus monkeys, both in the absence and presence of dietary cholesterol (0.3%, w/w). In all the purified diets, which contained 33%en as fat blends, myristic acid (14:0) and linoleic acid (18:2) were held constant at 0.3%en and 3.7%en, respectively. Cholesterol-free diets containing either high 18:1 (19%en), roughly equivalent levels of 16:0 and 18:1 (12 and 15%en, respectively), or a high level of 16:0 (18%en), generated similar values for total plasma cholesterol (TC), HDL-C and LDL-C. Plasma triacylglycerol concentrations (TG) were significantly higher when monkeys were fed the 16: 0-rich diet than when fed the 18: 1-rich diet (75 +/- 6 vs. 52 +/- 8 mg/dl; P < 0.05). LDL and HDL kinetic parameters (assessed after simultaneous injection of homologous 131I-LDL and 125I-HDL) revealed no significant differences between the 18: 1-rich or 16: 0-rich diets. By contrast, with added dietary cholesterol (0.78 mg/kcal) the 16: 0-rich diet resulted in significantly higher TC (318 +/- 20 vs. 299 +/- 20 mg/dl; P < 0.05) and LDL-C (136 +/- 10 vs. 117 +/- 10 mg/dl; P < 0.05) in comparison to the 18: 1-rich diet. HDL-C was unaffected (159 +/- 8 vs. 156 +/- 5 mg/dl), but plasma TG concentrations also tended to be higher (70 +/- 8 vs. 60 +/- 6 mg/dl, P < 0.08). Kinetic studies revealed that the higher LDL-C concentration was associated with an elevated pool size of LDL apo B (40 +/- 2 vs. 34 +/- 2 mg/kg body weight; P < 0.005), the latter attributed to decreased FCR (1.06 +/- 0.07 vs. 1.27 +/- 0.12 pools/day; P < 0.04) with no effect on the transport rate of LDL apo B (41 +/- 2 vs. 42 +/- 3 mg/kg body weight per day). HDL kinetic parameters were comparable during the 16: 0 and 18: 1 dietary periods, but dietary cholesterol caused an increase in apo A-I pool size and transport rate without impacting FCR. In this study a palmitic acid-rich diet failed to alter plasma or LDL-C when compared to an oleic acid-rich diet, unless the diet also contained cholesterol. In the latter case, 16: 0 increased LDL-C, which reflected a decrease in the efficiency of LDL apo B removal.
Khosla
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P
Foster Biomedical Research Laboratory, Brandeis University, Waltham, MA 02254.
Hayes
K C
KC
D000704:Analysis of Variance; D000818:Animals; D002428:Cebus; D002791:Cholesterol, Dietary / Q000097:blood / Q000494:pharmacology*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood*; D004041:Dietary Fats / Q000494:pharmacology*; D007700:Kinetics; D008055:Lipids / Q000097:blood; D008297:Male; D019301:Oleic Acid; D009829:Oleic Acids / Q000494:pharmacology*; D010169:Palmitic Acids / Q000494:pharmacology*; D011973:Receptors, LDL / Q000378:metabolism
D002791:Cholesterol, Dietary; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004041:Dietary Fats; D008055:Lipids; D009829:Oleic Acids; D010169:Palmitic Acids; D011973:Receptors, LDL; D019301:Oleic Acid