Minor components of pomace olive oil enhance VLDL-receptor expression in macrophages when treated with postprandial triglyceride-rich lipoproteins

J S Perona,L Sinausia,M Avella,E Montero,K M Botham,R Cabello-Moruno

doi:10.3989/gya.0109151

J S Perona, L Sinausia + Show 4 more

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https://doi.org/10.3989/gya.0109151

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Abstract

Pomace olive oil (POO) is rich in minor components, which can modulate the composition of postprandial triglyceride-rich lipoproteins (TRL) and their uptake by macrophages. The aim of the present study was to investigate the effects of postprandial TRL obtained after the ingestion of meals containing POO or refined olive oil (ROO) on foam cell formation, one of the initial steps of atherogenesis. Meals were administered to 9 healthy men and TRL were isolated from serum 4h after the intake. POO intake led to TRL with lower triglyceride/apo B48 and triglyceride/apo B100 ratios compared to ROO. Upon incubation of THP-1 macrophages with the TRL, an increase in the intracellular triglyceride content and foam cell formation was observed. Compared to ROO-TRL, the only receptor involved in lipoprotein uptake that showed changes in the mRNA expression after treatment with POO-TRL was the VLDL-receptor (VLDLr). In conclusion, the intake of POO modified the composition of human TRL, which increased the VLDLr gene expression in macrophages. However, the changes were not sufficient to enhance foam cell formation.

Highlights

It has become clear in the last years that postprandial lipemia, which is caused by raised levels of triglyceride-rich lipoproteins (TRL) present in the blood after a meal containing fat, may be a risk factor for atherosclerosis (Jackson et al, 2012)
No significant differences were observed in apo B48 and apo B100 concentrations in TRL after the intake of both dietary oils, but the lower TG content in TRL formed after Pomace olive oil (POO) ingestion led to particles with significantly lower TG/apo B48 and TG/ apo B100 ratios
In macrophages incubated with POOTRL intracellular accumulation of cholesteryl esters (CE) and free cholesterol (FC) was similar to that seen in control cells

Summary

Introduction

It has become clear in the last years that postprandial lipemia, which is caused by raised levels of triglyceride-rich lipoproteins (TRL) present in the blood after a meal containing fat, may be a risk factor for atherosclerosis (Jackson et al, 2012). TG are carried in the circulation by CM, which are synthesized in the intestine and transport fat of dietary origin (exogenous fat), and VLDL, which are synthesized and secreted by the liver (endogenous fat) (Jackson et al, 2012). The magnitude and duration of the postprandial TG response is influenced by a number of metabolic processes, including the rate of TG secretion from the intestine and the liver, the activity of enzymes involved in the TRL processing and the rate of clearance of TRL remnants by receptormediated pathways (Jackson et al, 2012). Minor lipid components from dietary fats are absorbed in the intestine to other lipids and they are incorporated into postprandial TRL for their transport in plasma. Once delivered to the tissues as part of TRL they may have important physiological effects (Perona et al, 2008)

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