Low density lipoprotein (LDL) oxidation (ox) is known to play a role in the development of atherosclerotic lesions. The dense LDL (dLDL) subtraction is more susceptible to oxidation and may be particularly atherogenic. However, dLDL is less readily protected by antioxidants such as vitamin E (E). Fatty acids (FA) in LDL isolated from subjects in US are only weakly correlated to extent of LDL ox. Yet, after extensive supplementation with monounsaturated fatty acids (MUFA) during metabolic studies, LDL and especially dLDL was protected from ox. It remains unclear, however, how relevant and how practical MUFA enrichment of the diet may be. Therefore, we chose a group of free living people in two coastal, northwestern towns of Greece known to produce and consume large amounts of olive oil, an oil high in MUFA, and evaluated the relationship of FA content to LDL and dLDL ox. Blood was drawn from 23 subjects, 15-71 years old, who were not taking antioxidants. LDL and dLDL subfractions were isolated and their E levels, FA composition, susceptibility to and extent of copper mediated ox was examined. Susceptibility to ox was estimated by the delay (lagtime) before rapid propagation of conjugated dienes (CD) and extent of ox by peak CD formation. The % of 18:1 and 18:2 FA in the LDL particles was different in Greek subjects vs. pooled data from US subjects (mean 24.5+/-2.8 vs. 18.5+/-1.6 for 18:1 and 36.9+/-3.5 vs. 40.2+/-2.0 for 18:2). The ratio of 18:1/18:2 in the Greek (0.66) vs. US subjects(0.45) was substantially higher. The mean level of LDL vit E was 9.4+2.5 ug/mg protein which is higher than that found in average US populations. A negative correlation was noted between 18:1 and extent of LDL CD formation, R=-0.51, p<0.02 and with LDL lagtimes, R=-0.47, p<0.02, and a positive correlation between 18:2 and extent of LDL CD formation, R=0.66, p<0.001. Importantly, a negative correlation was also found between 18:1 and extent of dLDL CD formation, R=-.0.77, p<0.001. There was no significant correlation of 18:2 or E to LDL or dLDL lagtimes. In summary, we have shown in a free living population eating a diet high in MUFA, that LDL is sufficiently enriched in MUFA and depleted in polyunsaturated FA to reduce LDL and dLDL susceptibility to ox and overall extent of ox. This demonstrates that diets high in MUFA are readily achievable, can inhibit LDL ox and may protect against atherosclerosis.
|Original language||English (US)|
|Journal||Journal of Investigative Medicine|
|State||Published - Jan 1 1996|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)