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

Lassel, Taous; Guérin, Maryse; Auboiron, Silvy; Chapman, M. John; Guy‐Grand, Bernard

doi:10.1161/01.atv.18.1.65

Cited by 43 publications

(35 citation statements)

References 63 publications

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“…For each subject, a postprandial time course was performed following consumption of a solid mixed meal that provided a total of 1,200 kcal (14% protein, 38% carbohydrate, and 48% fat) as previously described ( 5 ). Subjects were asked to abstain from alcohol and vigorous exercise for 24 h before the day of the test.…”

Section: Subjects and Postprandial Time Coursementioning

confidence: 99%

Postprandial lipemia enhances the capacity of large HDL2 particles to mediate free cholesterol efflux via SR-BI and ABCG1 pathways in type IIB hyperlipidemia

Julia

Duchêne

Fournier

et al. 2010

Journal of Lipid Research

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This article is available online at http://www.jlr.org Supplementary key words ATP binding cassette transporter G1 • high density lipoprotein • cellular cholesterol effl ux • scavenger receptor class B, type I Elevated postprandial hypertriglyceridemia is a characteristic metabolic disorder associated with increased cardiovascular risk ( 1 ). After ingestion of dietary fat, an increase in plasma triglyceridemia is observed, refl ecting transient accumulation of plasma triglyceride-rich lipoproteins (TRL) of intestinal and hepatic origin, namely, apoB48-containing chylomicrons (CM), apoB100-containing very low density lipoprotein (VLDL), and their remnants. The systemic accumulation of these particles represents a pro-atherogenic consequence of the postprandial period, as they can penetrate the arterial intima at sites of endothelial dysfunction, with retention by the extracellular matrix, thereby contributing to cholesterol accumulation and plaque formation ( 2 ). During the postprandial phase, plasma cholesteryl ester transfer protein (CETP) activity is enhanced as a result of an increase in circulating cholesteryl ester (CE) acceptors and/or CETP concentrations ( 3, 4 ). On a quantitative basis, both CM and large VLDL-1 particles represent the preferential acceptors of CE from HDL among TRL during the postprandial phase ( 5 ). This process favors CE enrichment of TRL Abstract Lipid and cholesterol metabolism in the postprandial phase is associated with both quantitative and qualitative remodeling of HDL particle subspecies that may infl uence their anti-atherogenic functions in the reverse cholesterol transport pathway. We evaluated the capacity of whole plasma or isolated HDL particles to mediate cellular free cholesterol (FC) effl ux, cholesteryl ester transfer protein (CETP)-mediated cholesteryl ester (CE) transfer, and selective hepatic CE uptake during the postprandial phase in subjects displaying type IIB hyperlipidemia (n = 16). Postprandial, large HDL2 displayed an enhanced capacity to mediate FC effl ux via both scavenger receptor class B type I (SR-BI)-dependent (+12%; P < 0.02) and ATP binding cassette transporter G1 (ABCG1)-dependent (+31%; P < 0.008) pathways in in vitro cell systems. In addition, the capacity of whole postprandial plasma (4 h and 8 h postprandially) to mediate cellular FC effl ux via the ABCA1-dependent pathway was signifi cantly increased (+19%; P < 0.0003). Concomitantly, postprandial lipemia was associated with elevated endogenous CE transfer rates from HDL2 to apoB lipoproteins and with attenuated capacity ( ؊ 17%; P < 0.02) of total HDL to deliver CE to hepatic cells. Postprandial lipemia enhanced SR-BI and ABCG1-dependent effl ux to large HDL2 particles. However, postprandial lipemia is equally associated with deleterious features by enhancing formation of CE-enriched, triglyceride-rich lipoprotein particles through the action of CETP and by reducing the direct return of HDL-CE to the liver. -Julia, Z., E. Duchene, N. Fournier, N. Bellanger, M. J. Chapman, W. Le Goff, and M...

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Section: Subjects and Postprandial Time Coursementioning

confidence: 99%

Postprandial lipemia enhances the capacity of large HDL2 particles to mediate free cholesterol efflux via SR-BI and ABCG1 pathways in type IIB hyperlipidemia

Julia

Duchêne

Fournier

et al. 2010

Journal of Lipid Research

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“…The largest TRL (Sf . 400) do not seem to play a major role in this process, whereas the medium-to larger-sized TRLs seem to be more important [64]. The largest increase in cholesterol in the TRL fraction in the postprandial state is accounted for by an accumulation in VLDL [32].…”

Section: Intravascular Metabolism Of Trlmentioning

confidence: 99%

Postprandial lipoprotein metabolism and atherosclerosis

Karpe

1999

Journal of Internal Medicine

361

242

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“…This meal represented a typical Western meal of a total of 1,200 kcal and consisted of 14% protein, 38% carbohydrate, and 48% fat, providing 66 g fat and 142 mg cholesterol (26 Subjects were requested to abstain from alcohol and vigorous exercise for 24 h before the day of the test. For each subject, a baseline blood sample was collected at 8 AM after an overnight fasting period.…”

Section: Test Meal and Blood Samplesmentioning

confidence: 99%

Cholesteryl ester flux from HDL to VLDL-1 is preferentially enhanced in type IIB hyperlipidemia in the postprandial state

Guérin

Egger

Soudant

et al. 2002

Journal of Lipid Research

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Postprandial triglyceride-rich lipoproteins (TRL)exert proatherogenic effects at the arterial wall, including lipid deposition. Following consumption of a mixed meal (1,200 kcal), plasma-mediated cellular free cholesterol (FC) efflux, lecithin:cholesterol acyltransferase (LCAT), and cholesteryl ester transfer protein (CETP) activities were determined in subjects (n ‫؍‬ 12) displaying type IIB hyperlipidemia and compared with those in a normolipidemic control group (n ‫؍‬ 14). The relative capacity of plasma to induce FC efflux from Fu5AH cells via the SR-BI receptor was significantly increased 4 h postprandially ( ؉ 23%; P Ͻ 0.005) in the type IIB group, whereas it remained unchanged for postprandial plasma from normolipidemic subjects. LCAT activity was significantly elevated 2 h postprandially in both the IIB and control groups, ( ؉ 46% and ؉ 36%, respectively; P Ͻ 0.005 vs. respective baseline value). In type IIB subjects, total cholesteryl ester (CE) mass transfer from HDL to total TRL [chylomicrons (CMs) ؉ VLDL-1 ؉ VLDL-2 ؉ IDL] increased progressively from 15 ؎ 2 g CE/h/ml at baseline to 28 ؎ 2 g CE transferred/h/ml ( ؉ 87%; P ‫؍‬ 0.0004) at 4 h postprandially. CE transfer to CMs and VLDL-1 was preferentially stimulated (2.6-fold and 2.3-fold respectively) at 4 h in IIB subjects and occurred concomitantly with elevation in mass and particle number of both CMs (2.3-fold) and VLDL-1 (1.3-fold). Furthermore, in type IIB subjects, CETP-mediated total CE flux over the 8 h postprandial period from HDL to potentially atherogenic TRL was significantly enhanced, and notably to VLDL-1 (32-fold elevation; P Ͻ 0.005), relative to control subjects. Such CE transfer flux was reflected in a significant postprandial increase in CE-TG ratio in both CMs and VLDL-1 in type IIB plasmas. In conclusion, HDL-CE is preferentially targeted to VLDL-1 via the action of CETP during alimentary lipemia, thereby favoring formation and accumulation of atherogenic CE-rich remnant particles. In order to maintain cholesterol homeostasis in peripheral tissues, excess cellular cholesterol is returned to the liver for excretion via a multistep process termed "reverse cholesterol transport" (RCT) (1). A key component of this process involves the transfer of a significant portion of the cholesteryl ester (CE) pool in HDL to apoB-containing lipoproteins (VLDL, IDL, and LDL) via the action of the cholesteryl ester transfer protein (CETP) (2).Hyperlipidemia of phenotype IIB is associated with an increased risk of premature coronary artery disease and is characterized by concomitant elevation of circulating levels of atherogenic apoB-containing, triglyceride-rich (VLDL) and cholesterol-rich lipoproteins (VLDL remnants, IDL, and LDL including small, dense LDL) (3). In type IIB hyperlipidemia during the fasting state, CETP is implicated in the intravascular formation of atherogenic small, dense LDL through an indirect mechanism involving an elevated rate of CE transfer from HDL to VLDL, and more specifically, to large VLDL-1 particles (4, 5)....

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

Cited by 43 publications

References 63 publications

Postprandial lipemia enhances the capacity of large HDL2 particles to mediate free cholesterol efflux via SR-BI and ABCG1 pathways in type IIB hyperlipidemia

Postprandial lipemia enhances the capacity of large HDL2 particles to mediate free cholesterol efflux via SR-BI and ABCG1 pathways in type IIB hyperlipidemia

Postprandial lipoprotein metabolism and atherosclerosis

Cholesteryl ester flux from HDL to VLDL-1 is preferentially enhanced in type IIB hyperlipidemia in the postprandial state

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