Effect of virgin olive oil as spreadable preparation on atherosclerosis compared to dairy butter in Apoe-deficient mice

Abstract

Olive oil is the main source of lipid energy in the Mediterranean diet and there is strong evidence of its health benefits. The effect of extra virgin olive oil (EVOO) in the form of a preparation of spreadable virgin olive oil (S-VO) on the progression of atheroma plaques was investigated in Apoe-deficient mice, a model of accelerated atherosclerosis.

Methods: Two isocaloric Western purified diets containing 20% fat, either as S-VO or as dairy butter, were used to feed 28 males and 16 females of two-month-old Apoe-deficient mice for 12 weeks. S-VO was prepared by blending more than 75% virgin olive oil with other vegetal natural fat to obtain a solid fat. Plasma total cholesterol, triglycerides and HDL cholesterol were measured. Hepatic lipid droplets were analyzed. Areas of atherosclerotic aortic lesions were quantified in cross-sectional images of the proximal aorta and en face analysis of the whole aorta.

Results: Total plasma cholesterol was increased in mice on the butter-supplemented diet in both female and male mice compared to S-VO, and the ratio of TC/HDL-cholesterol was significantly lower in S-VO than in the butter diet, although only in males, and no differences in plasma triglycerides were observed. No significant differences in hepatic lipid droplets were observed between diets in either sex. Aortic lesion areas were significantly higher in mice consuming the butter versus the S-VO diet in both sexes.

Conclusion: Extra virgin olive oil prepared in spreadable form maintained the delay in atheroma plaque progression compared to butter.

Keywords: Apolipoprotein E deficient mice; Coronary artery disease (CAD); EVOO; Phenols.

Fig. 1

Physical aspect of S-VO (A). Experimental design and analytical methods used (B)

Fig. 2

Representative feed consumption (A), body weight monitoring during the dietary intervention (B). Animal weight gain (mg) in 12 weeks per feed intake (kcal) in males (C) and in females (D). Results are expressed as mean ± standard deviation. Statistical analysis was performed by Mann–Whitney test or Student's t-test based on normal distribution. *, p ≤ 0.05 butter vs. S-VO and **, p ≤ 0.01 butter vs. S-VO

Fig. 3

Representative fractions from FPLC profiles. Collected fractions analyzed for total cholesterol in males (A) and females (B). 13 to 17 fractions corresponded to VLDL, 18 to 24 to LDL, 25 to 29 to cholesterol-rich HDL and 30 to 33 to cholesterol-poor HDL

Fig. 4

Atherosclerotic lesions in the different experimental groups. Box and whiskers plots show the 5th to 95th percentile of individual aortic cross-sectional analysis (A). Representative images of aortic lesions at the valve level representative of each experimental condition (B). Presence of atherosclerotic foci as % of lesion en face study (C). ROC of cross-sectional areas in males and females (D). Statistical analyses were performed by Mann–Whitney test or t-Student test based on their normal distribution

Fig. 5

Correlation plots in males. Scatter plot of individual data of aortic atherosclerotic cross-sectional lesion versus body weight gain during the 12-week dietary intervention (A), and scatter plot of aortic cross-sectional lesion versus total cholesterol/HDL cholesterol ratio (B). Statistical correlations were performed using bilateral Spearman bivariate correlation analysis

Fig. 6

Correlation plots in females. Scatter plot of individual data of aortic atherosclerotic cross-sectional lesion vs. total cholesterol at the end of the 12-week dietary intervention. Statistical correlations were performed with bilateral Spearman bivariate correlation analysis