Triacylglycerol-rich lipoprotein margination: a potential surrogate for whole-body lipoprotein lipase activity and effects of eicosapentaenoic and docosahexaenoic acids.
BACKGROUND
Margination occurs when blood borne particles attach to the vessel wall. Triacylglycerol-rich lipoprotein (TRL) particles marginate when they bind to endothelial lipoprotein lipase (LpL).


OBJECTIVE
This study was undertaken to determine whether TRL margination reflects in vivo LpL activity and whether n-3 fatty acids affect fasting and fed TRL margination.


METHODS
Healthy subjects (n = 33) began with a 4-wk, placebo (olive oil; 4 g/d) run-in period and were then randomly assigned to 4 wk of treatment with 4 g/d of ethyl esters of either safflower oil (SAF; control), eicosapentaenoic acid (EPA), or docosahexaenoic acid (DHA). Margination volume (MV) was calculated by subtracting true from apparent plasma volume.


RESULTS
MVs were 3 times as great during the fasting state as during the fed state (P < 0.0001). In both the fasting and the fed states, MV was significantly correlated with plasma triacylglycerol and TRL half-lives. In the fed state, MV was also correlated with preheparin LpL, whereas in the fasting state it was not. There was no significant correlation between preheparin LpL and postheparin LpL in the fasting state. Relative to SAF, EPA and DHA supplementation resulted in higher MVs by 64% and 53% (both P < 0.001), respectively, in the fasting state, without significantly reducing fasting triacylglycerol concentrations. In the fed state, DHA doubled the MV (P < 0.05), whereas EPA had no significant effect.


CONCLUSIONS
The correlations between MV and TRL half-lives and preheparin LpL suggest that MV could be a reflection of whole-body LpL binding capacity. The increases in MVs with EPA and DHA supplementation suggest that these fatty acids may increase the amount of endothelial-bound LpL or its affinity for TRL.
Park
Yongsoon
Y
Lipid and Diabetes Research Center, Saint Luke's Hospital, and the University of Missouri-Kansas City School of Medicine, 64111, USA.
Jones
Philip G
PG
Harris
William S
WS
D000284:Administration, Oral; D000328:Adult; D000368:Aged; D001810:Blood Volume; D018592:Cross-Over Studies; D019587:Dietary Supplements; D004281:Docosahexaenoic Acids / Q000008:administration & dosage / Q000494:pharmacology; D004311:Double-Blind Method; D015118:Eicosapentaenoic Acid / Q000008:administration & dosage / Q000494:pharmacology; D005215:Fasting / Q000097:blood; D015525:Fatty Acids, Omega-3 / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D006493:Heparin / Q000378:metabolism; D006801:Humans; D006949:Hyperlipidemias / Q000178:diet therapy; D008071:Lipoprotein Lipase / Q000097:blood / Q000378:metabolism*; D008074:Lipoproteins / Q000378:metabolism*; D008297:Male; D008657:Metabolic Clearance Rate; D008875:Middle Aged; D019518:Postprandial Period / Q000502:physiology*; D012450:Safflower Oil / Q000008:administration & dosage / Q000737:chemistry; D014280:Triglycerides / Q000378:metabolism*
D015525:Fatty Acids, Omega-3; D008074:Lipoproteins; D014280:Triglycerides; D004281:Docosahexaenoic Acids; D012450:Safflower Oil; D006493:Heparin; D015118:Eicosapentaenoic Acid; D008071:Lipoprotein Lipase