Extra-virgin olive oil consumption improves the capacity of HDL to mediate cholesterol efflux and increases ABCA1 and ABCG1 expression in human macrophages

Abstract

The present study was aimed to investigate the effect of 12 weeks of extra-virgin olive oil (EVOO) consumption on the capacity of HDL to promote cholesterol efflux (CE) and to determine which CE pathways are modulated by EVOO consumption. Whole HDL and HDL 2 /HDL 3 subclasses were isolated from the plasma of twenty-six healthy volunteers before and after 12 weeks of EVOO consumption (25 ml/d). EVOO consumption increased the capacity of serum and HDL to mediate CE from THP-1, J774 macrophages and Fu5AH cells by 9·8-24·57 %, depending on the cell type. The increase in CE was independent of both HDL concentration and subclass distribution. The three HDL-mediated CE pathways (ATP-binding cassette (ABC) A1, ABCG1 and scavenger receptor class B type I (SR-BI)) were modulated by EVOO consumption. The fluidity of the phospholipidic layer of HDL increased by 13 % (P,0·001) following EVOO consumption compared with baseline. EVOO consumption also increased the release of excess cholesterol from human monocyte-derived macrophages (HMDM) by 44 % (P, 0·001), and ABCA1 and ABCG1 mRNA transcription by 16·08 % (P, 0·001) and 35·79 % (P, 0·01), respectively. The protein expression of these two cholesterol transporters also increased after EVOO consumption. In contrast, SR-BI mRNA and protein expression in HMDM were significantly lower after 12 weeks of EVOO consumption. Incubating J774 macrophages with EVOO polyphenol extracts induced a concentration-dependent up-regulation of ABCA1 and ABCG1 expression in macrophages. After 12 weeks of EVOO consumption, the capacity of HDL to mediate CE was improved and the ability of HMDM to release excess cholesterol was enhanced by increasing the expression of ABCA1 and ABCG1 transporters.

The intake of a high-fat diet and grape seed procyanidins induces gene expression changes in peripheral blood mononuclear cells of hamsters: capturing alterations in lipid and cholesterol metabolisms

“…Different studies have shown a modulation of the expression of cholesterol metabolism-related genes, such as abca1, abcg1 and srb1, in macrophages responding to treatment with polyphenols quercetin, resveratrol and extra virgin olive oil, another source of polyphenols (Voloshyna et al 2013;Lee et al 2013;Helal et al 2013). However, in our study, of all the analysed genes that are involved in cholesterol homoeostasis, only lss was up-regulated in PBMCs in response to the administration of GSPE in the STD-GSPE animals.…”

MediterrAsian Diet Products That Could Raise HDL-Cholesterol: A Systematic Review

“…Regarding the study design, out of the 15 studies, two were randomized, double-blind, placebo-controlled, and parallel-groups trials [32, 42], two were randomized, double-blind, and controlled clinical trials [30, 35], one was a randomized and double-blind trial [39], one was a randomized, controlled, and parallel study [44], one was a randomized, double-blind, and controlled crossover feeding trial [31], one was a randomized and single-blind crossover trial [33], two were randomized and controlled crossover studies [34, 38], one was a randomized and intervention crossover trial [36], two were double-blind crossover studies [37, 43], and two were pre-post studies [40, 41]. …”

“…Four studies [30, 33, 36, 42] included subjects with hypercholesterolemia or moderate hypercholesterolemia; seven studies [37–41, 43, 44] included subjects with normal lipid levels, one study [32] included subject with adherence to a vegetarian diet for at least one year, and two studies [34, 35] included healthy males and healthy volunteers.…”

Human paraoxonase 1 overexpression in mice stimulates HDL cholesterol efflux and reverse cholesterol transport

“…Cholesterol efflux was assessed by incubating the radiolabeled J774-macrophages for 4 h at 37°C with 50 μL/mL of apolipoprotein B-depleted plasma (PEG-treated plasma from wild-type or PON1-Tg mice)]; J774 macrophages transfected with hPON1 or MPM with 50 μg/mL of ApoA-1. The supernatants and the adherent cells (macrophages) were separated and prepared for [ 3 H]-cholesterol quantification as previously described by Loued et al [21]. A liquid scintillation counter was used to determine [ 3 H]-cholesterol level (counts/min or cpm) in both the supernatant and in macrophages (lysates).…”