Linoleic acid-rich fats reduce atherosclerosis development beyond its oxidative and inflammatory stress-increasing effect in apolipoprotein E-deficient mice in comparison with saturated fatty acid-rich fats

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<jats:p>The relative benefit of replacing saturated fatty acid with linoleic acids is still being debated because a linoleic acid-enriched diet increases oxidative and inflammatory stresses, although it is associated with a reduction in serum cholesterol levels. The present study was conducted to evaluate the effect of dietary supplementation of linoleic acid-rich (HL) fat, compared with a saturated fatty acid-rich (SF) fat on atherosclerotic lesion areas, serum and liver cholesterol levels, oxidative stress (urinary isoprostanes and serum malondialdehayde) and inflammatory stress (expression of aortic monocyte chemoattractant protein-1; MCP-1) in apo E-deficient mice. Male and female apo E-deficient mice (8 weeks old; seven to eight per group) were fed an AIN-76-based diet containing SF fat (50 g palm oil and 50 g lard/kg) or HL fat (100 g high-linoleic safflower-seed oil/kg) for 9 weeks. Compared with the SF diet, the HL diet lowered atherosclerosis (<jats:italic>P</jats:italic><0·05). It reduced serum total cholesterol levels (<jats:italic>P</jats:italic><0·05), increased HDL-cholesterol levels (<jats:italic>P</jats:italic><0·05) and lowered liver esterified cholesterol levels (<jats:italic>P</jats:italic><0·01). The HL diet-fed mice showed increased expression of MCP-1 mRNA (<jats:italic>P</jats:italic><0·05), serum levels of malondialdehayde (<jats:italic>P</jats:italic><0·05) and urinary excretion of 2,3-dinor-5,6-dihydro-8-iso-prostaglandin F2α;<jats:italic>P</jats:italic><0·05). These results suggest that having biomarkers<jats:italic>in vivo</jats:italic>for oxidative stress and inflammatory status of endothelial cells does not necessarily indicate predisposition to an increased lesion area in the aortic root in apo E-deficient mice fed an HL or SF diet.</jats:p>

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