Abstract
Abstract
Highlights
The long-term cholesterol-lowering effect of replacing intake of SFA with PUFA is well established, but has not been fully explained mechanistically
We examined the postprandial response of meals with different fat quality on expression of lipid genes in peripheral blood mononuclear cells (PBMC) in subjects with and without familial hypercholesterolaemia (FH)
At baseline (0 h), FH compared with control subjects had significantly lower expression of genes involved in fatty acid metabolism (ACACA, CPT1A and FADS1), cholesterol biosynthesis (FDPS), the gene coding for the scavenger receptor MSR1 and genes involved in the transcription of lipid genes (NR1H3 and SREBF2) (0·001 ≤ P ≤ 0·02) (Supplementary Table S1)
Summary
The long-term cholesterol-lowering effect of replacing intake of SFA with PUFA is well established, but has not been fully explained mechanistically. There was a significant interaction between meal and group for MSR1 (P = 0·03), where intake of SFA compared with n-6 PUFA induced a larger reduction in gene expression in controls only (P = 0·01). Intake of SFA compared with n-6 PUFA induced changes in gene expression of cholesterol influx and efflux mediators in PBMC including lower LDLR and higher ABCA1/G1, potentially explaining the long-term cholesterol-raising effect of a high SFA intake. Patients with familial hypercholesterolaemia (FH) are characterised by genetically elevated cholesterol levels, mainly due to a mutation in the gene coding for the LDL receptor (LDLR)(7) These patients have increased CVD mortality[8]. We recently showed that the postprandial TAG response did not differ between young FH subjects and healthy controls after intake of high-fat meals rich in SFA or PUFA. The TAG peaked later after intake of SFA compared with PUFA[11]
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