Tags

Type your tag names separated by a space and hit enter

Influence of apolipoprotein E polymorphism on apolipoprotein B-100 metabolism in normolipemic subjects.
J Clin Invest. 1991 Nov; 88(5):1490-501.JCI

Abstract

This study examined apolipoprotein (apo) B metabolism in normolipemic subjects homozygous for the apo E2 (n = 4), apo E3 (n = 5), or apo E4 (n = 5) phenotype. Radioiodinated very low density lipoprotein (VLDL1) (ultracentrifuge flotation rate [Sf] 60-400) and VLDL2 (Sf 20-60) were injected into volunteers and the conversion of apo B was followed through intermediate density lipoprotein (IDL) to low density lipoprotein (LDL). Subjects homozygous for E3 converted approximately 50% of LVDL2 to LDL, the remainder being lost by direct catabolism. Those with the E2 phenotype produced less VLDL1, but converted more of it to VLDL2 (compared to E3 subjects). They displayed a characteristic dyslipidemia with the presence of slowly catabolized VLDL1 and VLDL2 remnants. LDL levels were low owing to increased direct catabolism of VLDL2 and IDL and a reduced efficiency of delipidation; only 25% of VLDL2 apo B was directed to LDL production. In contrast, E4 subjects converted more VLDL2 apo B to LDL than E3 subjects. About 70% of VLDL2 apo B was found in LDL; direct catabolism of VLDL and IDL was reduced as was the fractional catabolic rate of LDL (0.2 vs. 0.26 in E3 subjects). These changes in the VLDL----IDL----LDL metabolic cascade can in part be explained by alterations in hepatic LDL receptors with E2 subjects having higher and E4 subjects lower activities than those in E3 homozygotes.

Authors+Show Affiliations

Institute of Clinical Biochemistry, Glasgow Royal Infirmary, Scotland.No 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

1939641

Citation

Demant, T, et al. "Influence of Apolipoprotein E Polymorphism On Apolipoprotein B-100 Metabolism in Normolipemic Subjects." The Journal of Clinical Investigation, vol. 88, no. 5, 1991, pp. 1490-501.
Demant T, Bedford D, Packard CJ, et al. Influence of apolipoprotein E polymorphism on apolipoprotein B-100 metabolism in normolipemic subjects. J Clin Invest. 1991;88(5):1490-501.
Demant, T., Bedford, D., Packard, C. J., & Shepherd, J. (1991). Influence of apolipoprotein E polymorphism on apolipoprotein B-100 metabolism in normolipemic subjects. The Journal of Clinical Investigation, 88(5), 1490-501.
Demant T, et al. Influence of Apolipoprotein E Polymorphism On Apolipoprotein B-100 Metabolism in Normolipemic Subjects. J Clin Invest. 1991;88(5):1490-501. PubMed PMID: 1939641.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Influence of apolipoprotein E polymorphism on apolipoprotein B-100 metabolism in normolipemic subjects. AU - Demant,T, AU - Bedford,D, AU - Packard,C J, AU - Shepherd,J, PY - 1991/11/1/pubmed PY - 1991/11/1/medline PY - 1991/11/1/entrez SP - 1490 EP - 501 JF - The Journal of clinical investigation JO - J Clin Invest VL - 88 IS - 5 N2 - This study examined apolipoprotein (apo) B metabolism in normolipemic subjects homozygous for the apo E2 (n = 4), apo E3 (n = 5), or apo E4 (n = 5) phenotype. Radioiodinated very low density lipoprotein (VLDL1) (ultracentrifuge flotation rate [Sf] 60-400) and VLDL2 (Sf 20-60) were injected into volunteers and the conversion of apo B was followed through intermediate density lipoprotein (IDL) to low density lipoprotein (LDL). Subjects homozygous for E3 converted approximately 50% of LVDL2 to LDL, the remainder being lost by direct catabolism. Those with the E2 phenotype produced less VLDL1, but converted more of it to VLDL2 (compared to E3 subjects). They displayed a characteristic dyslipidemia with the presence of slowly catabolized VLDL1 and VLDL2 remnants. LDL levels were low owing to increased direct catabolism of VLDL2 and IDL and a reduced efficiency of delipidation; only 25% of VLDL2 apo B was directed to LDL production. In contrast, E4 subjects converted more VLDL2 apo B to LDL than E3 subjects. About 70% of VLDL2 apo B was found in LDL; direct catabolism of VLDL and IDL was reduced as was the fractional catabolic rate of LDL (0.2 vs. 0.26 in E3 subjects). These changes in the VLDL----IDL----LDL metabolic cascade can in part be explained by alterations in hepatic LDL receptors with E2 subjects having higher and E4 subjects lower activities than those in E3 homozygotes. SN - 0021-9738 UR - https://www.unboundmedicine.com/medline/citation/1939641/Influence_of_apolipoprotein_E_polymorphism_on_apolipoprotein_B_100_metabolism_in_normolipemic_subjects_ L2 - https://doi.org/10.1172/JCI115459 DB - PRIME DP - Unbound Medicine ER -