The goal of this study was to investigate the effect of the dietary fat composition on LDL peak particle diameter. Therefore, we measured LDL size by gradient gel electrophoresis in 56 (30 men, 26 women) healthy participants in a controlled dietary study. First, all participants received a baseline diet rich in saturated fat for 2 wk; they were then randomly assigned to one of three dietary treatments, which contained refined olive oil [rich in monounsaturated fatty acids (MUFA), n = 18], rapeseed oil [rich in MUFA and (n-3)-polyunsaturated fatty acids (PUFA), n = 18], or sunflower oil [rich in (n-6)-PUFA, n = 20] as the principal source of fat for 4 wk. Repeated-measures ANOVA revealed a small, but significant reduction in LDL size during the oil diet phase (-0.36 nm, P = 0.012), which did not differ significantly among the three groups (P = 0.384). Furthermore, affiliation with one of the three diet groups did not contribute significantly to the observed variation in LDL size (P = 0.690). In conclusion, our data indicate that dietary unsaturated fat similarly reduces LDL size relative to saturated fat. However, the small magnitude of this reduction also suggests that the composition of dietary fat is not a major factor affecting LDL size.

BACKGROUND: There is lack of agreement on which dietary regimen is most suitable for treatment of hypertriglyceridemia, especially if high triglyceride concentrations are not due to obesity or alcohol abuse. We compared the effects on blood lipids of a diet high in total and unsaturated fat with a low-fat diet in patients with triglyceride concentrations of b 2.3 mmolal. METHODS: Nineteen non-obese male outpatients with triglycerides ranging from 2.30 to 9.94 mmolal received two consecutive diets for 3 weeks each: ®rst a modi®ed high-fat diet (39% total fat, 8% SFA, 15% monounsaturated fatty acids, 1.6% marine n-3 polyunsaturated fatty acids), and then a low-fat diet (total fat 28%, carbohydrates 54%). RESULTS: The high-fat diet signi®cantly decreased triglycerides (À63%), total cholesterol (À22%), VLDL cholesterol (À54%), LDL cholesterol (À16%), total apoC-III (À27%), apoC-III in apoB containing lipoproteins (apoC-III LpB; À31%) and in HDL (apoC-III nonLpB; À29%), apoE in serum (À33%) and apoB-containing lipoproteins (nonHDL-E; À42%), LpA-I (À16%), insulin (À36%), and leptin (À26%) and signi®cantly increased the means of HDL cholesterol ( 8%), LDL size ( 6%), lipoprotein lipase (LPL, 11%), hepatic lipase ( 13%), and lecithin: cholesterol acyltransferase (LCAT, 2%). The subsequent low-fat diet increased triglycerides ( 63%), VLDL cholesterol ( 19%), apoC-III ( 23%), apoC-III LpB ( 44%) apoC-III nonLpB ( 17%), apoE ( 29%) and nonHDL-E ( 43%), and decreased HDL cholesterol (À12%), LPL (À3%), and LCAT (À3%). Changes in triglycerides correlated with changes in LPL activity and insulin levels. CONCLUSIONS: In hypertriglyceridemic patients, a modi®ed diet rich in mono-and n-3 polyunsaturated fatty acids is more effective than a carbohydrate-rich low-fat diet in correcting the atherogenic lipoprotein phenotype.

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