Alimentary lipemia-induced redistribution of cholesteryl ester between lipoproteins. Studies in normolipidemic, combined hyperlipidemic, and hypercholesterolemic men.

Dullaart, Robin; Groener, J.E.M.; Wijk, H van; Sluiter, Wj; Erkelens, D. W.

doi:10.1161/01.atv.9.5.614

Cited by 49 publications

(12 citation statements)

References 39 publications

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“…45 Moreover, it has been proposed that the elevated plasma CETP levels observed in endogenous hyperlipidemia result in increased CETP gene expression by a mechanism similar to that involving dietary cholesterol. 46 These observations strongly suggest that elevation in CETP mass or activity during postprandial lipemia, as reported by others, 27,44 is above all the consequence of the amount of exogenous cholesterol consumed. In addition, the increase in plasma CETP levels observed by others 27,44 ranged from 5% to 12%, thereby suggesting heterogeneity in postprandial response in terms of increase in plasma CETP levels within normolipidemic subjects.…”

Section: Discussionsupporting

confidence: 63%

“…46 These observations strongly suggest that elevation in CETP mass or activity during postprandial lipemia, as reported by others, 27,44 is above all the consequence of the amount of exogenous cholesterol consumed. In addition, the increase in plasma CETP levels observed by others 27,44 ranged from 5% to 12%, thereby suggesting heterogeneity in postprandial response in terms of increase in plasma CETP levels within normolipidemic subjects. Similar conclusions may be reached from analysis of data with respect to changes in plasma CETP activity during postprandial lipemia.…”

Section: Discussionsupporting

confidence: 63%

“…In addition, Dullaart et al 43 demonstrated a minor increase (5%) in plasma CE transfer activity using an exogenous CE donor and acceptor particle system after a 140 g fat load. It is of interest that increase in plasma CETP activity 23 as well as in plasma CETP mass 44 during postprandial lipemia in normolipidemic subjects occurred after a high cholesterol meal in which the cholesterol content was approximately 600 mg. As shown by studies in human-CETP transgenic mice, a high cholesterol diet induces increase of transcription of the CETP gene. 45 Such upregulation of CETP gene expression in response to cholesterol requires the presence of natural flanking regions of the human CETP gene.…”

Section: Discussionmentioning

confidence: 99%

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Preferential Cholesteryl Ester Acceptors Among Triglyceride-Rich Lipoproteins During Alimentary Lipemia in Normolipidemic Subjects

Lassel

Guérin

Auboiron

et al. 1998

ATVB

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Abstract-Triglyceride-rich lipoproteins (TRLs), namely chylomicrons (CMs), VLDL, and their remnants, are implicated in the atherogenic features of postprandial lipemia. In human plasma, cholesteryl ester transfer protein (CETP) mediates the heteroexchange of neutral lipids, ie, triglycerides (TG) and cholesteryl esters (CE), between distinct subpopulations of apoB-and of apoAI-containing lipoproteins. In fasting normolipidemic plasma, CETP plays an antiatherogenic role by promoting preferential CE redistribution from HDL to LDL particles of intermediate subclass with optimal binding affinity for the cellular LDL receptor. While the relative proportions and chemical compositions of donor and acceptor lipoproteins are known to influence CETP activity, elevated levels of TRL present during alimentary lipemia have been proposed to be associated with enhanced CETP activity. To identify the preferential CE acceptor particles among postprandial TRL subfractions, we investigated the effects of a typical Western meal (1200 kcal, 14% protein; 38% carbohydrate; and 48% fat, monounsaturated/polyunsaturated ratio 4:1) on the rates of postprandial CE transfer from HDL to apoB-containing lipoproteins in normolipidemic subjects (nϭ13). Two hours postprandially, plasma levels of TRL were significantly elevated (140 versus 51 mg/dL at baseline, Pϭ.0001). Total rates of CE transferred (88Ϯ7 g ⅐ h Ϫ1 ⅐ mL Ϫ1 ) from HDL to apoB-containing lipoproteins were not significantly modified by alimentary lipemia over a period of 8 hours. Quantitatively, LDL accepted 64Ϯ5 g CE per hour per milliliter plasma from HDL, whereas CM (SfϾ400), VLDL1 (Sf 60 to 400), VLDL2 (Sf 20 to 60), and IDL (Sf 12 to 20) accepted 5Ϯ3, 16Ϯ3, 1.4Ϯ0.3, and 1.5Ϯ0.2, respectively. Quantitatively, VLDL1 was the major CE acceptor among TRLs (Pϭ.0001); thus, VLDL1, but not CMs, represented the major CE acceptor among TRLs. Qualitatively however, VLDL2 and IDL displayed a higher capacity to accept CE from HDL (51.6Ϯ4.1 and 46.3Ϯ2.8 g CE transferred per hour per milligram lipoprotein, respectively; PϽ.005) compared with CM, VLDL1, and LDL (12.6Ϯ2.8, 34.7Ϯ4.2, and 22.7Ϯ2.0 g CE transferred per hour per milligram lipoprotein, respectively). In conclusion, elevated postprandial TRL levels are not associated with enhanced total CE transfer to these particles. Furthermore, the qualitative features of postprandial CE transfer from HDL to CM and VLDL1 were not related to the relative TG content of these particles. The CETP-facilitated enrichment of VLDL1 in CE therefore identifies them as potentially atherogenic particles during the postprandial phase. (Arterioscler Thromb Vasc Biol. 1998;18:65-74.)

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Section: Discussionsupporting

confidence: 63%

Section: Discussionsupporting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Preferential Cholesteryl Ester Acceptors Among Triglyceride-Rich Lipoproteins During Alimentary Lipemia in Normolipidemic Subjects

Lassel

Guérin

Auboiron

et al. 1998

ATVB

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“…However, because humans will be mostly PP lipemic during the day owing to consumption of regular meals, LCAT-and CETP-mediated transformation of UC on cell membranes into chylomicron CEs may occur throughout the PP lipemic period in vivo. A number of studies [38][39][40] have shown PP chylomicronemia to be accompanied by a significant net decrease in LDL and HDL CE level as well as total plasma CE levels or a significant shift in the distribution of CEs from LDL and HDL to PP chylomicrons. The PP decreases in LDL and HDL CE levels were proportional to the increases of plasma TGs in PP plasma or the amount of fat ingested.…”

Section: Discussionmentioning

confidence: 99%

Potencies of Lipoproteins in Fasting and Postprandial Plasma to Accept Additional Cholesterol Molecules Released From Cell Membranes

Chung

Franklin

Cho

et al. 1998

ATVB

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Abstract-To investigate the role of various lipoproteins in plasma to promote cholesterol efflux from cell membranes, potencies of lipoproteins in normolipidemic fasting and postprandial (PP) plasmas to accept additional cholesterol molecules from cell membranes were determined. We used red blood cells (RBCs) PϽ0.20). In fasting plasma containing a low level of VLDL and HDL, isolated chylomicrons supplemented to the plasma were Ϸ9ϫ more potent than HDL in boosting the capacity of plasma to promote cholesterol efflux from RBCs. This study indicates that chylomicrons in PP plasma are the most potent ultimate acceptors of cholesterol released from cell membranes and that a low HDL level is not a factor that limits the ability of PP plasma to promote cholesterol efflux from cell membranes. Our data obtained from an in vitro system suggest that PP chylomicrons may play a major role in promoting reverse cholesterol transport in vivo, since the transfer of cholesterol from cell membranes to chylomicrons will lead to the rapid removal of this cholesterol by the liver. of UC between cell membranes and lipoproteins can be disturbed by an enzyme, lecithin:cholesterol acyltransferase (LCAT), which can lower the levels of UC on the lipoprotein surface by converting it into cholesterol ester (CE) and subsequently trapping the CEs in the cores of lipoproteins. Thus, LCAT-mediated generation of a UC gradient between cell membranes and lipoproteins allows a net transfer of cholesterol from cell membranes into lipoproteins. A major feature of the role of HDL in RCT promotion is its ability to serve as a major substrate for LCAT.

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“…It has also been reported that CEs that were first transferred from HDL to LDL were then transferred secondarily to CMs during PP phases (9). Induction of PP lipemia accompanies an increase in the plasma activities of both LCAT and CETP (15)(16)(17) and a net decrease in CE levels on both LDL and HDL, as well as in plasma total CE levels (18), and a shift in the distribution of CEs from endogenous lipoproteins to CMs (19). These observations suggest that CMs appearing in PP plasma may serve as acceptors of CEs from both LDL and HDL.…”

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confidence: 96%

Postprandial chylomicrons

Chung

Liang

Doran

et al. 2004

Journal of Lipid Research

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Reverse cholesterol transport (RCT), a process of transporting cholesterol from cell membranes to the liver for its excretion, occurs in the plasma compartment in vivo. Both lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer proteins (CETPs) may play an important role in regulating the rate of RCT by influencing the rate at which cholesterol released from cell membranes into plasma is trapped in the core of HDL via esterification and the rate at which the trapped HDL-cholesteryl ester (CE) is then transferred to apolipoprotein B (apoB)-containing lipoproteins for delivery to the liver (1-3). CETP promotes the transfer of CE from HDL to various apoB-containing lipoproteins [LDL, VLDL, IDL, and chylomicrons (CMs)] in plasma (3-9), but the catabolic rate and fate of these various apoB-containing lipoproteins differ in vivo (10). Thus, the rate of RCT promoted by LCAT and CETP might then depend on the rate and extent of transfer of HDL-CE to various apoB-containing lipoproteins in plasma in vivo. Although the extent of in vivo transfer of CE from HDL to various apoB-containing lipoproteins is known to be influenced by the levels of individual apoB-containing lipoproteins in plasma (11), the rate and potencies of the various apoB-containing lipoproteins to accept CE from HDL in vivo have not yet been fully elucidated. An earlier study (12) examining the fate of [ 3 H]CE-labeled HDL injected into fasting humans showed that 3 H-labeled CE on HDL appeared more rapidly on VLDL than on LDL. In rabbits, 3 H-labeled CE on

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Alimentary lipemia-induced redistribution of cholesteryl ester between lipoproteins. Studies in normolipidemic, combined hyperlipidemic, and hypercholesterolemic men.

Cited by 49 publications

References 39 publications

Preferential Cholesteryl Ester Acceptors Among Triglyceride-Rich Lipoproteins During Alimentary Lipemia in Normolipidemic Subjects

Preferential Cholesteryl Ester Acceptors Among Triglyceride-Rich Lipoproteins During Alimentary Lipemia in Normolipidemic Subjects

Potencies of Lipoproteins in Fasting and Postprandial Plasma to Accept Additional Cholesterol Molecules Released From Cell Membranes

Postprandial chylomicrons

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