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Metabolsim of apoB and apoC lipoproteins in man: kinetic studies in normal and hyperlipoproteininemic subjects.
J Lipid Res 1978; 19(1):38-56JL

Abstract

The kinetics of apolipoproteins B and C were studied in 14 normal and hyperlipoproteinemic subjects after injection of exogenously (125)I-labeled very low density lipoprotein (VLDL) particles. Plasma radioactivities of apoB and apoC were determined over a period of 4 days in VLDL (d < 1.006) and total radioactivity in intermediate (IDL) (1.006 < d < 1.019), low (LDL) (1.019 < d < 1.063), and high (HDL) (1.063 < d < 1.21) density lipoproteins. The data were analyzed by the use of a model, developed mostly from these data, with the following results. The VLDL particle undergoes a series of incremental density changes, most likely due to a number of delipidation steps, during which apoB stays with the particle until the density reaches the IDL range. There is, however, a loss of apoC associated with these delipidation steps. In our normal subjects, all IDL apoB eventually becomes LDL. In our hyperlipemic subjects some of the apoB on IDL is also degraded directly. The apoC lost by VLDL and IDL recycles to HDL, and most of it is picked up again by newly synthesized VLDL. There is a slowdown of the stepwise delipidation process in all hyperlipemic individuals studied. Three additional features became apparent in the type III subjects. First, there is a significant increase (a factor of 2 compared to normal) in the apoB synthesis rate by way of VLDL; second, there is an induced direct apoB synthesis pathway by way of IDL (and/or LDL); third, a bypass of the regular stepwise VLDL delipidation pathway is induced by which VLDL particles lose apoC but none of their apoB, thereby forming a new particle with metabolic properties similar to LDL, but with a density still in the VLDL density range. Two type III patients treated with nicotinic acid and clofibrate showed a sharp decrease in their VLDL apoB synthesis rates. This was somewhat compensated by an increased IDL apoB synthesis rate. A type I patient on a medium chain triglyceride diet also showed a number of metabolic changes, including reduced VLDL apoB synthesis and the induction of considerable IDL and/or LDL apoB synthesis.

Authors

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Pub Type(s)

Journal Article

Language

eng

PubMed ID

202659

Citation

Berman, M, et al. "Metabolsim of apoB and apoC Lipoproteins in Man: Kinetic Studies in Normal and Hyperlipoproteininemic Subjects." Journal of Lipid Research, vol. 19, no. 1, 1978, pp. 38-56.
Berman M, Hall M, Levy RI, et al. Metabolsim of apoB and apoC lipoproteins in man: kinetic studies in normal and hyperlipoproteininemic subjects. J Lipid Res. 1978;19(1):38-56.
Berman, M., Hall, M., Levy, R. I., Eisenberg, S., Bilheimer, D. W., Phair, R. D., & Goebel, R. H. (1978). Metabolsim of apoB and apoC lipoproteins in man: kinetic studies in normal and hyperlipoproteininemic subjects. Journal of Lipid Research, 19(1), pp. 38-56.
Berman M, et al. Metabolsim of apoB and apoC Lipoproteins in Man: Kinetic Studies in Normal and Hyperlipoproteininemic Subjects. J Lipid Res. 1978;19(1):38-56. PubMed PMID: 202659.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Metabolsim of apoB and apoC lipoproteins in man: kinetic studies in normal and hyperlipoproteininemic subjects. AU - Berman,M, AU - Hall,M,3rd AU - Levy,R I, AU - Eisenberg,S, AU - Bilheimer,D W, AU - Phair,R D, AU - Goebel,R H, PY - 1978/1/1/pubmed PY - 1978/1/1/medline PY - 1978/1/1/entrez SP - 38 EP - 56 JF - Journal of lipid research JO - J. Lipid Res. VL - 19 IS - 1 N2 - The kinetics of apolipoproteins B and C were studied in 14 normal and hyperlipoproteinemic subjects after injection of exogenously (125)I-labeled very low density lipoprotein (VLDL) particles. Plasma radioactivities of apoB and apoC were determined over a period of 4 days in VLDL (d < 1.006) and total radioactivity in intermediate (IDL) (1.006 < d < 1.019), low (LDL) (1.019 < d < 1.063), and high (HDL) (1.063 < d < 1.21) density lipoproteins. The data were analyzed by the use of a model, developed mostly from these data, with the following results. The VLDL particle undergoes a series of incremental density changes, most likely due to a number of delipidation steps, during which apoB stays with the particle until the density reaches the IDL range. There is, however, a loss of apoC associated with these delipidation steps. In our normal subjects, all IDL apoB eventually becomes LDL. In our hyperlipemic subjects some of the apoB on IDL is also degraded directly. The apoC lost by VLDL and IDL recycles to HDL, and most of it is picked up again by newly synthesized VLDL. There is a slowdown of the stepwise delipidation process in all hyperlipemic individuals studied. Three additional features became apparent in the type III subjects. First, there is a significant increase (a factor of 2 compared to normal) in the apoB synthesis rate by way of VLDL; second, there is an induced direct apoB synthesis pathway by way of IDL (and/or LDL); third, a bypass of the regular stepwise VLDL delipidation pathway is induced by which VLDL particles lose apoC but none of their apoB, thereby forming a new particle with metabolic properties similar to LDL, but with a density still in the VLDL density range. Two type III patients treated with nicotinic acid and clofibrate showed a sharp decrease in their VLDL apoB synthesis rates. This was somewhat compensated by an increased IDL apoB synthesis rate. A type I patient on a medium chain triglyceride diet also showed a number of metabolic changes, including reduced VLDL apoB synthesis and the induction of considerable IDL and/or LDL apoB synthesis. SN - 0022-2275 UR - https://www.unboundmedicine.com/medline/citation/202659/Metabolsim_of_apoB_and_apoC_lipoproteins_in_man:_kinetic_studies_in_normal_and_hyperlipoproteininemic_subjects_ L2 - http://www.jlr.org/cgi/pmidlookup?view=long&amp;pmid=202659 DB - PRIME DP - Unbound Medicine ER -