Lipidomic changes of LDL after consumption of Camelina sativa oil, fatty fish and lean fish in subjects with impaired glucose metabolism—A randomized controlled trial

Arja T Erkkilä,Suvi Manninen,Linda Fredrikson,Monika Bhalke,Minna Holopainen,Maija Ruuth,Maria Lankinen,Reijo Käkelä,Katariina Öörni,Ursula S Schwab

doi:10.1016/j.jacl.2021.08.060

Abstract

BackgroundThere is little knowledge on the effects of alpha-linolenic acid (ALA) and n-3 long-chain polyunsaturated fatty acids (n-3 LCPUFA) on the LDL lipidome and aggregation of LDL particles. ObjectiveWe examined if consumption of Camelina sativa oil (CSO) as a source of ALA, fatty fish (FF) as a source of n-3 LCPUFA and lean fish (LF) as a source of fish protein affect the lipidome of LDL as compared to a control diet. MethodsParticipants with impaired glucose tolerance (39 women and 40 men) were randomized to 4 study groups (CSO providing 10 g/d ALA, FF and LF [both 4 fish meals/wk] and control limiting their fish and ALA intake) in a 12-week, parallel trial. Diets were instructed and dietary fats were provided to the participants. The lipidome of LDL particles isolated from samples collected at baseline and after intervention was analyzed with electrospray ionization-tandem mass spectrometry. ResultsIn the CSO group, the relative concentrations of saturated and monounsaturated cholesteryl ester species in LDL decreased and the species with ALA increased. In the FF group, LDL phosphatidylcholine (PC) species containing n-3 LCPUFA increased. There was a significant positive correlation between the change in total sphingomyelin and change in LDL aggregation, while total PC and triunsaturated PC species were inversely associated with LDL aggregation when all the study participants were included in the analysis. ConclusionDietary intake of CSO and FF modifies the LDL lipidome to contain more polyunsaturated and less saturated lipid species. The LDL surface lipids are associated with LDL aggregation.

Highlights

Plant-derived alpha-linolenic acid (ALA, 18:3n-3) decreases serum LDL cholesterol concentration,[1] while n-3 long chain polyunsaturated (LCPUFAs), eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n3) from marine sources reduce serum triglyceride (TG; used when triacylglycerols [TAG] are measured by glyceroldetecting assay) concentration and in high supplemental doses they are suggested to even increase LDL cholesterol.[2,3,4]The core of LDL particles consists of mostly cholesteryl ester (CE) molecules, and there are some TAG.[5]
We have previously reported that the diet with Camelina sativa oil (CSO) reduced serum total and LDL cholesterol concentrations[1] and the diet with fatty fish (FF) caused a shift towards larger HDL particles.[13]
Our aim was to examine if consumption of CSO, FF and lean fish (LF) affect the lipidome of LDL as compared to the control diet and further whether specific components of the LDL lipidome are associated with serum lipid concentrations and the tendency of LDL to aggregate

Summary

Introduction

Plant-derived alpha-linolenic acid (ALA, 18:3n-3) decreases serum LDL cholesterol concentration,[1] while n-3 long chain polyunsaturated (LCPUFAs), eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n3) from marine sources reduce serum triglyceride (TG; used when triacylglycerols [TAG] are measured by glyceroldetecting assay) concentration and in high supplemental doses they are suggested to even increase LDL cholesterol.[2,3,4]The core of LDL particles consists of mostly cholesteryl ester (CE) molecules, and there are some TAG (triacylglycerol is used when the intact molecules e.g. detected by mass spectrometry are addressed).[5]. Plant-derived alpha-linolenic acid (ALA, 18:3n-3) decreases serum LDL cholesterol concentration,[1] while n-3 long chain polyunsaturated (LCPUFAs), eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n3) from marine sources reduce serum triglyceride (TG; used when triacylglycerols [TAG] are measured by glyceroldetecting assay) concentration and in high supplemental doses they are suggested to even increase LDL cholesterol.[2,3,4]. Padro and coworkers showed that low-fat milk supplemented with n-3 LCPUFA increased n-3 LCPUFA proportions in LDL CE and increased the ratio of PC 36:5 to lysophosphatidylcholine (LPC) 16:0, which is suggested to be an anti-inflammatory change.[6] Consumption of DHA-enriched high-oleic acid (18:1n-9) canola oil increased the proportion of DHA in LDL CE.[7]. Objective: We examined if consumption of Camelina sativa oil (CSO) as a source of ALA, fatty fish (FF) as a source of n-3 LCPUFA and lean fish (LF) as a source of fish protein affect the lipidome of LDL as compared to a control diet

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