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Effects of simvastatin on apoB metabolism and LDL subfraction distribution.
Arterioscler Thromb. 1993 Feb; 13(2):170-89.AT

Abstract

Seven moderately hypercholesterolemic subjects were studied before and after 10 weeks of simvastatin therapy (20 mg/day). Therapy reduced low density lipoprotein (LDL) cholesterol by 39% (p < 0.001), whereas high density lipoprotein and very low density lipoprotein (VLDL) cholesterol were unchanged. Apolipoprotein (apo) B-containing lipoproteins were divided into VLDL1 (Sf 60-400), VLDL2 (Sf 20-60), intermediate density lipoprotein (IDL) (Sf 12-20), and LDL (Sf 0-12), and metabolic changes were sought in dual-tracer VLDL1 and VLDL2 turnover studies. VLDL1 apoB pool size was unaltered by therapy, as were its rates of synthesis, catabolism, and delipidation to VLDL2. Similarly, the VLDL2 apoB pool size was unchanged, but its metabolic fate was altered. The IDL pool size fell significantly (27%, p < 0.01) due entirely to an increased fractional catabolism of the lipoprotein. In our subjects, the circulating mass of LDL apoB decreased (49%, p < 0.01) primarily due to a reduction in its synthesis. Before therapy, 30% of the apoB entering the delipidation cascade in these hyperlipidemic subjects was converted to LDL. On therapy the input remained the same, but direct catabolism from VLDL2 and IDL was increased (p < 0.05), and as a result only 16% eventually appeared in LDL. These kinetic changes were associated with a fall in particle cholesteryl ester content throughout the delipidation cascade. We also observed a link between LDL kinetics and its subfraction distribution. Simvastatin influences the metabolism of LDL, IDL, and VLDL2 but not VLDL1.

Authors+Show Affiliations

Institute of Biochemistry, Glasgow Royal Infirmary, UK.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8427854

Citation

Gaw, A, et al. "Effects of Simvastatin On apoB Metabolism and LDL Subfraction Distribution." Arteriosclerosis and Thrombosis : a Journal of Vascular Biology, vol. 13, no. 2, 1993, pp. 170-89.
Gaw A, Packard CJ, Murray EF, et al. Effects of simvastatin on apoB metabolism and LDL subfraction distribution. Arterioscler Thromb. 1993;13(2):170-89.
Gaw, A., Packard, C. J., Murray, E. F., Lindsay, G. M., Griffin, B. A., Caslake, M. J., Vallance, B. D., Lorimer, A. R., & Shepherd, J. (1993). Effects of simvastatin on apoB metabolism and LDL subfraction distribution. Arteriosclerosis and Thrombosis : a Journal of Vascular Biology, 13(2), 170-89.
Gaw A, et al. Effects of Simvastatin On apoB Metabolism and LDL Subfraction Distribution. Arterioscler Thromb. 1993;13(2):170-89. PubMed PMID: 8427854.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of simvastatin on apoB metabolism and LDL subfraction distribution. AU - Gaw,A, AU - Packard,C J, AU - Murray,E F, AU - Lindsay,G M, AU - Griffin,B A, AU - Caslake,M J, AU - Vallance,B D, AU - Lorimer,A R, AU - Shepherd,J, PY - 1993/2/1/pubmed PY - 1993/2/1/medline PY - 1993/2/1/entrez SP - 170 EP - 89 JF - Arteriosclerosis and thrombosis : a journal of vascular biology JO - Arterioscler Thromb VL - 13 IS - 2 N2 - Seven moderately hypercholesterolemic subjects were studied before and after 10 weeks of simvastatin therapy (20 mg/day). Therapy reduced low density lipoprotein (LDL) cholesterol by 39% (p < 0.001), whereas high density lipoprotein and very low density lipoprotein (VLDL) cholesterol were unchanged. Apolipoprotein (apo) B-containing lipoproteins were divided into VLDL1 (Sf 60-400), VLDL2 (Sf 20-60), intermediate density lipoprotein (IDL) (Sf 12-20), and LDL (Sf 0-12), and metabolic changes were sought in dual-tracer VLDL1 and VLDL2 turnover studies. VLDL1 apoB pool size was unaltered by therapy, as were its rates of synthesis, catabolism, and delipidation to VLDL2. Similarly, the VLDL2 apoB pool size was unchanged, but its metabolic fate was altered. The IDL pool size fell significantly (27%, p < 0.01) due entirely to an increased fractional catabolism of the lipoprotein. In our subjects, the circulating mass of LDL apoB decreased (49%, p < 0.01) primarily due to a reduction in its synthesis. Before therapy, 30% of the apoB entering the delipidation cascade in these hyperlipidemic subjects was converted to LDL. On therapy the input remained the same, but direct catabolism from VLDL2 and IDL was increased (p < 0.05), and as a result only 16% eventually appeared in LDL. These kinetic changes were associated with a fall in particle cholesteryl ester content throughout the delipidation cascade. We also observed a link between LDL kinetics and its subfraction distribution. Simvastatin influences the metabolism of LDL, IDL, and VLDL2 but not VLDL1. SN - 1049-8834 UR - https://www.unboundmedicine.com/medline/citation/8427854/Effects_of_simvastatin_on_apoB_metabolism_and_LDL_subfraction_distribution_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&amp;PAGE=linkout&amp;SEARCH=8427854.ui DB - PRIME DP - Unbound Medicine ER -