Cholesteryl ester flux from HDL to VLDL-1 is preferentially enhanced in type IIB hyperlipidemia in the postprandial state
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 est...
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| Format: | Article |
| Language: | English |
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Elsevier
2002-10-01
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| Series: | Journal of Lipid Research |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S002222752032784X |
| _version_ | 1818444364115869696 |
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| author | Maryse Guerin Pascal Egger Céline Soudant Wilfried Le Goff Arie van Tol Reynald Dupuis M.John Chapman |
| author_facet | Maryse Guerin Pascal Egger Céline Soudant Wilfried Le Goff Arie van Tol Reynald Dupuis M.John Chapman |
| author_sort | Maryse Guerin |
| collection | DOAJ |
| description | 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 < 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 < 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 μg CE/h/ml at baseline to 28 ± 2 μg 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 < 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. |
| first_indexed | 2024-12-14T19:14:45Z |
| format | Article |
| id | doaj.art-57ab962875b84169b6073f82eebb031a |
| institution | Directory Open Access Journal |
| issn | 0022-2275 |
| language | English |
| last_indexed | 2024-12-14T19:14:45Z |
| publishDate | 2002-10-01 |
| publisher | Elsevier |
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| series | Journal of Lipid Research |
| spelling | doaj.art-57ab962875b84169b6073f82eebb031a2022-12-21T22:50:39ZengElsevierJournal of Lipid Research0022-22752002-10-01431016521660Cholesteryl ester flux from HDL to VLDL-1 is preferentially enhanced in type IIB hyperlipidemia in the postprandial stateMaryse Guerin0Pascal Egger1Céline Soudant2Wilfried Le Goff3Arie van Tol4Reynald Dupuis5M.John Chapman6Institut National de la Santé et de la Recherche Médicale, INSERM Unité 551, Dyslipoproteinemia and Atherosclerosis, Hôpital de la Pitié, 75651 Paris, France; Department of Biochemistry, Erasmus University, Rotterdam, The Netherlands; Pfizer, Paris, FranceInstitut National de la Santé et de la Recherche Médicale, INSERM Unité 551, Dyslipoproteinemia and Atherosclerosis, Hôpital de la Pitié, 75651 Paris, France; Department of Biochemistry, Erasmus University, Rotterdam, The Netherlands; Pfizer, Paris, FranceInstitut National de la Santé et de la Recherche Médicale, INSERM Unité 551, Dyslipoproteinemia and Atherosclerosis, Hôpital de la Pitié, 75651 Paris, France; Department of Biochemistry, Erasmus University, Rotterdam, The Netherlands; Pfizer, Paris, FranceInstitut National de la Santé et de la Recherche Médicale, INSERM Unité 551, Dyslipoproteinemia and Atherosclerosis, Hôpital de la Pitié, 75651 Paris, France; Department of Biochemistry, Erasmus University, Rotterdam, The Netherlands; Pfizer, Paris, FranceInstitut National de la Santé et de la Recherche Médicale, INSERM Unité 551, Dyslipoproteinemia and Atherosclerosis, Hôpital de la Pitié, 75651 Paris, France; Department of Biochemistry, Erasmus University, Rotterdam, The Netherlands; Pfizer, Paris, FranceInstitut National de la Santé et de la Recherche Médicale, INSERM Unité 551, Dyslipoproteinemia and Atherosclerosis, Hôpital de la Pitié, 75651 Paris, France; Department of Biochemistry, Erasmus University, Rotterdam, The Netherlands; Pfizer, Paris, FranceInstitut National de la Santé et de la Recherche Médicale, INSERM Unité 551, Dyslipoproteinemia and Atherosclerosis, Hôpital de la Pitié, 75651 Paris, France; Department of Biochemistry, Erasmus University, Rotterdam, The Netherlands; Pfizer, Paris, FrancePostprandial 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 < 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 < 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 μg CE/h/ml at baseline to 28 ± 2 μg 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 < 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.http://www.sciencedirect.com/science/article/pii/S002222752032784Xcholesteryl ester transfer proteinatherosclerosislecithin:cholesterol acyltransferasecellular cholesterol efflux |
| spellingShingle | Maryse Guerin Pascal Egger Céline Soudant Wilfried Le Goff Arie van Tol Reynald Dupuis M.John Chapman Cholesteryl ester flux from HDL to VLDL-1 is preferentially enhanced in type IIB hyperlipidemia in the postprandial state Journal of Lipid Research cholesteryl ester transfer protein atherosclerosis lecithin:cholesterol acyltransferase cellular cholesterol efflux |
| title | Cholesteryl ester flux from HDL to VLDL-1 is preferentially enhanced in type IIB hyperlipidemia in the postprandial state |
| title_full | Cholesteryl ester flux from HDL to VLDL-1 is preferentially enhanced in type IIB hyperlipidemia in the postprandial state |
| title_fullStr | Cholesteryl ester flux from HDL to VLDL-1 is preferentially enhanced in type IIB hyperlipidemia in the postprandial state |
| title_full_unstemmed | Cholesteryl ester flux from HDL to VLDL-1 is preferentially enhanced in type IIB hyperlipidemia in the postprandial state |
| title_short | Cholesteryl ester flux from HDL to VLDL-1 is preferentially enhanced in type IIB hyperlipidemia in the postprandial state |
| title_sort | cholesteryl ester flux from hdl to vldl 1 is preferentially enhanced in type iib hyperlipidemia in the postprandial state |
| topic | cholesteryl ester transfer protein atherosclerosis lecithin:cholesterol acyltransferase cellular cholesterol efflux |
| url | http://www.sciencedirect.com/science/article/pii/S002222752032784X |
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