Persistent abnormalities in lipoprotein composition and cholesteryl ester transfer following lovastatin treatment.
Optimally effective lipid-lowering agents should not only restore plasma lipids to normal levels but also correct potentially atherogenic alterations in lipoprotein composition and function often present in hyperlipidemic patients. Lovastatin, a competitive inhibitor of cholesterol biosynthesis, cle...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
1990-07-01
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| Series: | Journal of Lipid Research |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0022227520426355 |
| _version_ | 1818942974864654336 |
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| author | JD Bagdade JT Lane N Stone MC Ritter PV Subbaiah |
| author_facet | JD Bagdade JT Lane N Stone MC Ritter PV Subbaiah |
| author_sort | JD Bagdade |
| collection | DOAJ |
| description | Optimally effective lipid-lowering agents should not only restore plasma lipids to normal levels but also correct potentially atherogenic alterations in lipoprotein composition and function often present in hyperlipidemic patients. Lovastatin, a competitive inhibitor of cholesterol biosynthesis, clearly lowers plasma cholesterol levels. Its effects on lipoprotein composition and cholesteryl ester transfer (CET), a key step in reverse cholesterol transport, however, are not known. Since abnormalities in CET and lipoprotein composition are present in patients with hypercholesterolemia, we studied these parameters of plasma lipoprotein transport in twelve hypercholesterolemic (HC; Type IIa) subjects (six male, six female) before and 2 months after lovastatin treatment (20 mg qd). Before lovastatin, the free cholesterol (FC)/lecithin (L) ratio in plasma, a new index of cardiovascular risk that reflects lipoprotein surface composition, was abnormally increased (1.18 +/- 0.26 vs controls 0.83 +/- 0.14; P less than 0.001) in very low density lipoproteins (VLDL) and high density lipoprotein-3 (HDL3), and remained so after treatment despite significant declines in whole plasma cholesterol (311.7 +/- 68.2 vs 215.6 +/- 27.2 mg/dl; P less than 0.001), low density lipoprotein (LDL)-cholesterol (206.3 +/- 47.9 vs 146.8 +/- 29.4; P less than 0.001), and apolipoprotein B (149 +/- 30 vs 110 +/- 17; P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS) |
| first_indexed | 2024-12-20T07:19:58Z |
| format | Article |
| id | doaj.art-2a946c45be4d446493645bde22c58c69 |
| institution | Directory Open Access Journal |
| issn | 0022-2275 |
| language | English |
| last_indexed | 2024-12-20T07:19:58Z |
| publishDate | 1990-07-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Lipid Research |
| spelling | doaj.art-2a946c45be4d446493645bde22c58c692022-12-21T19:48:42ZengElsevierJournal of Lipid Research0022-22751990-07-0131712631269Persistent abnormalities in lipoprotein composition and cholesteryl ester transfer following lovastatin treatment.JD Bagdade0JT Lane1N Stone2MC Ritter3PV Subbaiah4Department of Medicine, Rush Medical College, Chicago, IL.Department of Medicine, Rush Medical College, Chicago, IL.Department of Medicine, Rush Medical College, Chicago, IL.Department of Medicine, Rush Medical College, Chicago, IL.Department of Medicine, Rush Medical College, Chicago, IL.Optimally effective lipid-lowering agents should not only restore plasma lipids to normal levels but also correct potentially atherogenic alterations in lipoprotein composition and function often present in hyperlipidemic patients. Lovastatin, a competitive inhibitor of cholesterol biosynthesis, clearly lowers plasma cholesterol levels. Its effects on lipoprotein composition and cholesteryl ester transfer (CET), a key step in reverse cholesterol transport, however, are not known. Since abnormalities in CET and lipoprotein composition are present in patients with hypercholesterolemia, we studied these parameters of plasma lipoprotein transport in twelve hypercholesterolemic (HC; Type IIa) subjects (six male, six female) before and 2 months after lovastatin treatment (20 mg qd). Before lovastatin, the free cholesterol (FC)/lecithin (L) ratio in plasma, a new index of cardiovascular risk that reflects lipoprotein surface composition, was abnormally increased (1.18 +/- 0.26 vs controls 0.83 +/- 0.14; P less than 0.001) in very low density lipoproteins (VLDL) and high density lipoprotein-3 (HDL3), and remained so after treatment despite significant declines in whole plasma cholesterol (311.7 +/- 68.2 vs 215.6 +/- 27.2 mg/dl; P less than 0.001), low density lipoprotein (LDL)-cholesterol (206.3 +/- 47.9 vs 146.8 +/- 29.4; P less than 0.001), and apolipoprotein B (149 +/- 30 vs 110 +/- 17; P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)http://www.sciencedirect.com/science/article/pii/S0022227520426355 |
| spellingShingle | JD Bagdade JT Lane N Stone MC Ritter PV Subbaiah Persistent abnormalities in lipoprotein composition and cholesteryl ester transfer following lovastatin treatment. Journal of Lipid Research |
| title | Persistent abnormalities in lipoprotein composition and cholesteryl ester transfer following lovastatin treatment. |
| title_full | Persistent abnormalities in lipoprotein composition and cholesteryl ester transfer following lovastatin treatment. |
| title_fullStr | Persistent abnormalities in lipoprotein composition and cholesteryl ester transfer following lovastatin treatment. |
| title_full_unstemmed | Persistent abnormalities in lipoprotein composition and cholesteryl ester transfer following lovastatin treatment. |
| title_short | Persistent abnormalities in lipoprotein composition and cholesteryl ester transfer following lovastatin treatment. |
| title_sort | persistent abnormalities in lipoprotein composition and cholesteryl ester transfer following lovastatin treatment |
| url | http://www.sciencedirect.com/science/article/pii/S0022227520426355 |
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