Abstract

Pequi is the fruit of Caryocar brasiliense and its oil has a high concentration of monounsaturated and saturated fatty acids, which are anti- and pro-atherogenic agents, respectively, and of carotenoids, which give it antioxidant properties. Our objective was to study the effect of the intake of a cholesterol-rich diet supplemented with pequi oil, compared to the same diet containing soybean oil, on atherosclerosis development, and oxidative stress in atherosclerosis-susceptible LDL receptor-deficient mice (LDLr−/−, C57BL/6-background). Female mice were fed a cholesterol-rich diet containing 7% soybean oil (Soybean group, N = 12) or 7% pequi oil (Pequi group, N = 12) for 6 weeks. The Pequi group presented a more atherogenic lipid profile and more advanced atherosclerotic lesions in the aortic root compared to the Soybean group. However, the Pequi group presented a less advanced lesion in the aorta than the Soybean group and showed lower lipid peroxidation (Soybean group: 50.2 ± 7.1; Pequi group: 30.0 ± 4.8 µmol MDA/mg protein) and anti-oxidized LDL autoantibodies (Soybean group: 35.7 ± 9.4; Pequi group: 15.6 ± 3.7 arbitrary units). Peritoneal macrophages from the Pequi group stimulated with zymosan showed a reduction in the release of reactive oxygen species compared to the Soybean group. Our data suggest that a pequi oil-rich diet slows atherogenesis in the initial stages, possibly due to its antioxidant activity. However, the increase of serum cholesterol induces a more prominent LDL migration toward the intimae of arteries, increasing the advanced atherosclerotic plaque. In conclusion, pequi oil associated with an atherogenic diet worsens the lipid profile and accelerates the formation of advanced atherosclerotic lesions despite its antioxidant action.

Highlights

  • Atherosclerosis is a multifactorial disease in which genetic, environmental, and lifestyle risk factors drive the lipid abnormalities that determine the progression of atherosclerosis under the action of oxidative stress, inflammation, and thrombogenicity

  • There was a significant increase in the concentration of low-density lipoprotein (LDL) cholesterol by pequi oil-supplemented diet ingestion, we found lower levels of circulating oxidized LDL (oxLDL) antibody in pequi oil-fed animals (Figure 3), supporting the antioxidant effect of pequi oil seen in the liver

  • The proportion of monounsaturated fatty acids (MUFA) in pequi oil did not appear to be adequate to counteract the effects of saturated fatty acid (SFA) on blood lipids

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Summary

Introduction

Atherosclerosis is a multifactorial disease in which genetic, environmental, and lifestyle risk factors drive the lipid abnormalities that determine the progression of atherosclerosis under the action of oxidative stress, inflammation, and thrombogenicity. Saturated fatty acids increase low-density lipoprotein (LDL) cholesterol by inhibiting LDL receptor activity and enhancing apolipoprotein B-containing lipoprotein production [1]. Replacement of saturated fat with polyunsaturated fat has been shown to decrease total cholesterol (TC) and LDL cholesterol by lowering LDL cholesterol production rates and/ or increasing LDL clearance rates. Replacement of saturated fat with polyunsaturated fat has been shown to decrease high-density lipoprotein (HDL) cholesterol, it decreases LDL cholesterol to even a greater extent, with a consequent reduction of the LDL/HDL ratio. Replacement of saturated fat with monounsaturated fat has been associated with decreased TC and LDL cholesterol, but the magnitude of HDL reduction is lower than when polyunsaturated fats are the replacement nutrient [2,3,4]

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