Abstract
Triglyceride (TG) enrichment of high density lipoprotein (HDL), which occurs in hypertriglyceridemic states, significantly enhances the rate at which HDL apolipoprotein (apo)A-I is cleared from the circulation of healthy humans. In the New Zealand White (NZW) rabbit, a species naturally deficient in hepatic lipase (HL), TG enrichment of HDL requires prior lipolytic modification to enhance apoA-I clearance. However, the effect of TG enrichment of HDL on the subsequent clearance of HDL cholesteryl ester (CE) has not previously been examined in vivo. Therefore, we investigated, in the NZW rabbit, the effect of ex vivo TG enrichment of rabbit HDL (by incubation with human very low density lipoprotein) on the clearance of HDL CE and apoA-I radiolabeled with 3H-cholesteryl oleyl ether and with 131I, respectively. In nine experiments, TG enrichment of rabbit HDL resulted in an 87% average increase in HDL TG and a corresponding 31% reduction in HDL CE content. The calculated apoA-I and CE fractional catabolic rates associated with TG-rich versus fasting HDL tracers were not significantly different (apoA-I: 0.119 ± 0.017 vs. 0.107 ± 0.024 pools per h, P = 0.68; CE: 0.147 ± 0.014 vs. 0.114 ± 0.019 pools per h, P = 0.20). In an animal model deficient in HL, TG enrichment of HDL did not alter the rates of HDL apoA-I or selective CE clearance. Further studies are needed to determine whether, in the presence of HL, TG enrichment of HDL alters selective HDL CE clearance. —Rashid, S., K. D. Uffelman, P. H. R. Barrett, P. Vicini, K. Adeli, and G. F. Lewis. Triglyceride enrichment of HDL does not alter HDL-selective cholesteryl ester clearance in rabbits.
Highlights
Triglyceride (TG) enrichment of high density lipoprotein (HDL), which occurs in hypertriglyceridemic states, significantly enhances the rate at which HDL apolipoproteinA-I is cleared from the circulation of healthy humans
We have previously demonstrated in humans that triglyceride (TG) enrichment of HDL markedly enhances the clearance of HDL-associated apolipoproteinA-I from the circulation [7]
TG enrichment of rabbit HDL with human ver y low density lipoproteins (VLDL) resulted in a large (87%) increase in HDL TG content (P Ͻ 0.0001) in the TG-rich HDL tracer compared with the fasting HDL tracer
Summary
Triglyceride (TG) enrichment of high density lipoprotein (HDL), which occurs in hypertriglyceridemic states, significantly enhances the rate at which HDL apolipoprotein (apo)A-I is cleared from the circulation of healthy humans. The effect of TG enrichment of HDL on the subsequent clearance of HDL cholesteryl ester (CE) has not previously been examined in vivo. We investigated, in the NZW rabbit, the effect of ex vivo TG enrichment of rabbit HDL (by incubation with human very low density lipoprotein) on the clearance of HDL CE and apoA-I radiolabeled with 3H-cholesteryl oleyl ether and with 131I, respectively. Triglyceride enrichment of HDL does not alter HDL-selective cholesteryl ester clearance in rabbits. Most in vivo studies to date that have examined the effect of hypertriglyceridemia on HDL metabolism have focused on the kinetics of HDL-associated apoA-l, the major protein component of the HDL particle [6]. Recent in vitro studies investigating the effect of TG enrichment of HDL, as occurs in hypertriglyceridemic states, on the process of selective CE uptake have shown opposing results.
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