P. Khosla et Kc. Hayes, DIETARY PALMITIC ACID RAISES PLASMA LDL CHOLESTEROL RELATIVE TO OLEIC-ACID ONLY AT A HIGH INTAKE OF CHOLESTEROL, Biochimica et biophysica acta, 1210(1), 1993, pp. 13-22
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 l
ipoprotein metabolism was investigated in 12 normocholesterolemic cebu
s 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 blen
ds, myristic acid (14:0) and linoleic acid (18:2) were held constant a
t 0.3%en and 3.7%en, respectively. Cholesterol-free diets containing e
ither high 18:1 (19%en), roughly equivalent levels of 16:0 and 18:1 (1
2 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. Pl
asma triacylglycerol concentrations (TG) were significantly higher whe
n 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 (as
sessed after simultaneous injection of homologous I-131-LDL and I-125-
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<0.0
5) 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 hig
her (70+/-8 vs. 60+/-6 mg/dl, P<0.08). Kinetic studies revealed that t
he higher LDL-C concentration was associated with an elevated pool siz
e of LDL apo B (40+/-2 vs. 34+/-2 mg/kg body weight; P<0.005), the lat
ter 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 compa
rable during the 16:0 and 18:1 dietary periods, but dietary cholestero
l caused an increase in apo A-I pool size and transport rate without i
mpacting 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 d
iet also contained cholesterol. In the latter case, 16:0 increased LDL
-C, which reflected a decrease in the efficiency of LDL apo B removal.