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Correspondence to:
Perry Colvin.
Large LpAI HDL particles, containing only apoA-I without apoA-II, are reported to be the major anti-atherogenic portion of HDL and to be increased in individuals with low risk for coronary heart disease. To determine whether the plasma concentration of large LpAI is modulated by the rate of production or catabolism of apolipoprotein A-I (apoA-I) in large LpAI, kinetic studies of large LpAI were performed in African green monkeys consuming an atherogenic diet with either high plasma HDL concentration (120 ± 36 mg/dl, mean ± SD, n = 3) or low plasma HDL concentration (40 ± 13 mg/dl, n = 3). Large LpAI was isolated, without ultracentrifugation, by immunoaffinity and gel filtration and radiolabeled. After injection, the specific activity of apoA-I in large HDL, consisting of both LpAI and LpAI:AII particles, was followed. A multicompartmental model was developed for the kinetics of apoA-I in large HDL, which indicated that a portion of large HDL is distributed to a sequestered pool, outside the circulating plasma, and reenters circulating plasma approximately 3 h after injection. There was no conversion of large LpAI to smaller HDL particles or transfer of radiolabeled apoA-I to smaller HDL particles. Although the mean fractional catabolic rate was not different comparing the high and low HDL group, the mean production rate of apoA-I in large HDL was 4 -fold greater in the high HDL group compared with the low HDL group.
These data support the hypothesis that the plasma concentration of large HDL is controlled primarily by the rate of production of apoA-I in large HDL.—Colvin, P., E. Moriguchi, H. Barrett, J. Parks, and L. Rudel. Production rate determines plasma concentration of large high density lipoprotein in non-human primates. J. Lipid Res. 1998. 39: 2076–2085.
Supplementary key words:
high density lipoprotein, LpAI, LpA-I:A-II, apolipoprotein A-I, catabolism, kinetic model
Copyright © 1998 by Lipid Research, Inc.
Production rate determines plasma concentration of large high density lipoprotein in non-human primates
Perry Colvinb,
Emilio Moriguchia,
Hugh Barrettc,
John Parksa, and
Larry Rudela
a Department of Comparative Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157
b Department of Internal Medicine, Division of Gerontology, University of Maryland School of Medicine and the Baltimore Veterans Affairs Medical Center, Geriatrics Research, Education, and Clinical Center, Baltimore, MD 21201
c Department of Bioengineering, University of Washington, Seattle, WA 98195
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