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Plasma kinetics of VLDL and HDL apoC-I in normolipidemic and hypertriglyceridemic subjects.
J Lipid Res. 2002 Oct; 43(10):1680-7.JL

Abstract

ApoC-I has several different lipid-regulating functions including, inhibition of receptor-mediated uptake of plasma triglyceride-rich lipoproteins, inhibition of cholesteryl ester transfer activity, and mediation of tissue fatty acid uptake. Since little is known about the rate of production and catabolism of plasma apoC-I in humans, the present study was undertaken to determine the plasma kinetics of VLDL and HDL apoC-I using a primed constant (12 h) intravenous infusion of deuterium-labeled leucine. Data were obtained for 14 subjects: normolipidemics (NL, n = 4), hypertriglyceridemics (HTG, n = 4) and combined hyperlipidemics (CHL, n = 6). Plasma VLDL triglyceride (TG) levels were 0.59 +/- 0.03, 4.32 +/- 0.77 (P < 0.01 vs. NL), and 2.20 +/- 0.39 mmol/l (P < 0.01 vs. NL), and plasma LDL cholesterol (LDL-C) levels were 2.34 +/- 0.22, 2.48 +/- 0.26, and 5.35 +/- 0.48 mmol/l (P < 0.01 vs. NL), respectively. HTG and CHL had significantly (P < 0.05) increased levels of total plasma apoC-I (12.5 +/- 1.2 and 12.4 +/- 1.3 mg/dl, respectively) versus NL (7.9 +/- 0.6 mg/dl), due to significantly (P < 0.01) elevated levels of VLDL apoC-I (5.8 +/- 0.8 and 4.5 +/- 0.8 vs. 0.3 +/- 0.1 mg/dl). HTG and CHL also had increased rates of VLDL apoC-I transport (i.e., production) versus NL: 2.29 +/- 0.34 and 3.04 +/- 0.53 versus 0.24 +/- 0.11 mg/kg.day (P < 0.01), with no significant change in VLDL apoC-I residence times (RT): 1.16 +/- 0.12 versus 0.69 +/- 0.06 versus 0.74 +/- 0.17. Although HDL apoC-I concentrations were not significantly lower in HTG and CHL versus NL, HDL apoC-I rates of transport were inversely related to plasma and VLDL-TG levels (r = -0.63 and -0.62, respectively, P < 0.05). Our results demonstrate that increased levels of plasma and VLDL apoC-I in hypertriglyceridemic subjects (with or without elevated LDL-C levels) are associated with increased levels of plasma VLDL apoC-I production.

Authors+Show Affiliations

Hyperlipidemia and Atherosclerosis Research Group, Montréal, Québec, Canada. cohnj@ircm.qc.caNo 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

12364552

Citation

Cohn, Jeffrey S., et al. "Plasma Kinetics of VLDL and HDL apoC-I in Normolipidemic and Hypertriglyceridemic Subjects." Journal of Lipid Research, vol. 43, no. 10, 2002, pp. 1680-7.
Cohn JS, Tremblay M, Batal R, et al. Plasma kinetics of VLDL and HDL apoC-I in normolipidemic and hypertriglyceridemic subjects. J Lipid Res. 2002;43(10):1680-7.
Cohn, J. S., Tremblay, M., Batal, R., Jacques, H., Veilleux, L., Rodriguez, C., Bernier, L., Mamer, O., & Davignon, J. (2002). Plasma kinetics of VLDL and HDL apoC-I in normolipidemic and hypertriglyceridemic subjects. Journal of Lipid Research, 43(10), 1680-7.
Cohn JS, et al. Plasma Kinetics of VLDL and HDL apoC-I in Normolipidemic and Hypertriglyceridemic Subjects. J Lipid Res. 2002;43(10):1680-7. PubMed PMID: 12364552.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Plasma kinetics of VLDL and HDL apoC-I in normolipidemic and hypertriglyceridemic subjects. AU - Cohn,Jeffrey S, AU - Tremblay,Michel, AU - Batal,Rami, AU - Jacques,Hélène, AU - Veilleux,Lyne, AU - Rodriguez,Claudia, AU - Bernier,Lise, AU - Mamer,Orval, AU - Davignon,Jean, PY - 2002/10/5/pubmed PY - 2003/3/21/medline PY - 2002/10/5/entrez SP - 1680 EP - 7 JF - Journal of lipid research JO - J Lipid Res VL - 43 IS - 10 N2 - ApoC-I has several different lipid-regulating functions including, inhibition of receptor-mediated uptake of plasma triglyceride-rich lipoproteins, inhibition of cholesteryl ester transfer activity, and mediation of tissue fatty acid uptake. Since little is known about the rate of production and catabolism of plasma apoC-I in humans, the present study was undertaken to determine the plasma kinetics of VLDL and HDL apoC-I using a primed constant (12 h) intravenous infusion of deuterium-labeled leucine. Data were obtained for 14 subjects: normolipidemics (NL, n = 4), hypertriglyceridemics (HTG, n = 4) and combined hyperlipidemics (CHL, n = 6). Plasma VLDL triglyceride (TG) levels were 0.59 +/- 0.03, 4.32 +/- 0.77 (P < 0.01 vs. NL), and 2.20 +/- 0.39 mmol/l (P < 0.01 vs. NL), and plasma LDL cholesterol (LDL-C) levels were 2.34 +/- 0.22, 2.48 +/- 0.26, and 5.35 +/- 0.48 mmol/l (P < 0.01 vs. NL), respectively. HTG and CHL had significantly (P < 0.05) increased levels of total plasma apoC-I (12.5 +/- 1.2 and 12.4 +/- 1.3 mg/dl, respectively) versus NL (7.9 +/- 0.6 mg/dl), due to significantly (P < 0.01) elevated levels of VLDL apoC-I (5.8 +/- 0.8 and 4.5 +/- 0.8 vs. 0.3 +/- 0.1 mg/dl). HTG and CHL also had increased rates of VLDL apoC-I transport (i.e., production) versus NL: 2.29 +/- 0.34 and 3.04 +/- 0.53 versus 0.24 +/- 0.11 mg/kg.day (P < 0.01), with no significant change in VLDL apoC-I residence times (RT): 1.16 +/- 0.12 versus 0.69 +/- 0.06 versus 0.74 +/- 0.17. Although HDL apoC-I concentrations were not significantly lower in HTG and CHL versus NL, HDL apoC-I rates of transport were inversely related to plasma and VLDL-TG levels (r = -0.63 and -0.62, respectively, P < 0.05). Our results demonstrate that increased levels of plasma and VLDL apoC-I in hypertriglyceridemic subjects (with or without elevated LDL-C levels) are associated with increased levels of plasma VLDL apoC-I production. SN - 0022-2275 UR - https://www.unboundmedicine.com/medline/citation/12364552/Plasma_kinetics_of_VLDL_and_HDL_apoC_I_in_normolipidemic_and_hypertriglyceridemic_subjects_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2275(20)32787-5 DB - PRIME DP - Unbound Medicine ER -