Alterations of HDL cholesterol distribution induced by incubation of human serum

Gambert, Philippe; Lallemant, Christian; Athias, Anne; Padieu, P

doi:10.1016/0005-2760(82)90159-x

Cited by 62 publications

(11 citation statements)

References 17 publications

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“…On the basis of the findings of a number of investigators (Castro & Fielding, 1988;Cheung & Wolf, 1989;Dieplinger et al, 1985;Eisenberg et al, 1978;Francone et al, 1989;Gambert et al, 1982;Holmquist & Carlson, 1985;Hopkins & Barter, 1984;Hopkins et al, 1985;Jonas et al, 1988Jonas et al, , 1990Lagrost et al, 1990;Nichols et al, 1981Nichols et al, , 1984Nichols et al, ,1985Nichols et al, , 1987Rajaram & Barter, 1986;Roheim, 1986;Rose & Ellerbe, 1982) as well as our own, we have assembled a model in which apoA-I cycles between pre-P-HDL and a-HDL in connection with the movement of cholesteryl esters through HDL (Figure 9) (Kunitake et al, 1992). As free cholesterol, derived from donors, enters the HDL and is esterified by 1ecithin:cholesterol acyltransferase (LCAT), pre-P-HDL are converted into a-HDL.…”

Section: Discussionmentioning

confidence: 97%

Apolipoprotein A-I-containing lipoproteins, with or without apolipoprotein A-II, as progenitors of pre-.beta. high-density lipoprotein particles

Hennessy¹,

Kunitake²,

Kane³

1993

Biochemistry

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Apolipoprotein A-I-(apoA-I-) containing lipoproteins isolated by immunoaffinity chromatography can be divided into two general subfractions on the basis of the presence [Lp(AI + AII)] or absence [Lp(AI - AII)] of apoA-II. The Lp(AI - AII) subfraction can be further subfractionated into two subgroups with pre-beta mobility as well as those of alpha mobility. We have characterized the Lp(AI - AII) and Lp(AI + AII) subfractions after the removal of pre-beta high-density lipoproteins (pre-beta-HDL) to compare only the two subfractions with alpha mobility. The Lp(AI - AII) and Lp(AI + AII) of alpha mobility, while both heterogeneous subfractions, share many gross features in common. Both subfractions were predominantly spherical in shape, had similar conformation of apoA-I as investigated by circular dichroism and specific endoproteases, and had similar contents of phospholipids, phospholipid species, triglycerides, and cholesterol ester. However, there was significantly less protein (-10%) and more free cholesterol (+46%) in the Lp(AI - AII) subfraction than in the Lp(AI + AII) subfraction. We investigated the generation of pre-beta-HDL from both the Lp(AI - AII) and Lp(AI + AII) subfractions during incubation with low-density lipoproteins and cholesteryl ester transfer protein. We found that both Lp(AI - AII) and Lp(AI + AII) subfractions were capable of generating pre-beta-HDL-like particles. Our results suggest that the formation of pre-beta-HDL involves dissociation of apoA-I from both Lp(AI - AII) and Lp(AI + AII) subfractions. These results refine a model describing the cycling of apoA-I between pre-beta-HDL and alpha-HDL linked to the movement of cholesteryl esters through HDL.

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Section: Discussionmentioning

confidence: 97%

Apolipoprotein A-I-containing lipoproteins, with or without apolipoprotein A-II, as progenitors of pre-.beta. high-density lipoprotein particles

Hennessy¹,

Kunitake²,

Kane³

1993

Biochemistry

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“…Total and unesteri®ed cholesterol were measured by gas liquid chromatography of the bis (trimethylsilyl) tri¯uoro-acetamide/trimethyl chlorosilane derivatives [22,23]. Esteri®ed cholesterol concentrations were obtained by subtraction (total cholesterol minus unesteri®ed cholesterol).…”

Section: Chemical Analysismentioning

confidence: 99%

Low birth weight at term impairs cord serum lipoprotein compositions and concentrations

Merzouk

Bouchenak

El-Korso

et al. 1998

European Journal of Pediatrics

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“…The size and distribution of LDL and HDL particles were determined on Sudan Black prestained plasma by 2 ± 20% polyacrylamide linear gradient gel electrophoresis followed by densitometric scanning of the gels at 590 nm [14]. Subjects were classi®ed into three groups on the basis of distinct LDL subclass patterns [15]: pattern A, major LDL peak §27.4 nm, pattern B, major LDL peak ¦26.2 nm, pattern I, major LDL peak around 26.8 nm.…”

Section: Methodsmentioning

confidence: 99%

Effects of fish oil fatty acids on plasma lipids and lipoproteins and oxidant-antioxidant imbalance in healthy subjects

Foulon¹

1999

Scandinavian Journal of Clinical and Laboratory Investigation

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The purpose of this study was to investigate the effect of eicosapentaenoic and docosahexaenoic acids on plasma lipids and lipoproteins, lipid peroxidation and antioxidant status in healthy humans. A total of 19 healthy volunteers consumed 6 g/day Maxepa fish oil for 3 weeks (1.8 g n-3 fatty acids/day). At baseline and at day 21, we evaluated plasma lipoproteins, plasma and low-density lipoprotein fatty acids, lipid peroxidation markers (malondialdehyde concentration, low-density lipoprotein peroxidation in vitro), and the content of a number of antioxidants (reduced and oxidized glutathione in whole blood, plasma and erythrocyte glutathione peroxidases, plasma vitamin E and beta carotene). Plasma concentrations of total cholesterol, triglycerides, phospholipids, low-density lipoprotein cholesterol and low-density lipoprotein size did not differ significantly after 3 weeks of supplementation. Adding the fish oil to the diet increased the concentration of n-3 very-long-chain polyunsaturated fatty acids and decreased the concentration of n-6 fatty acid and oleic acid in plasma and low-density lipoprotein. Eicosapentaenoic and docosahexaenoic acid supplementation caused elevated values of the high-density lipoprotein cholesterol due to an increment of the high-density lipoprotein 2 fraction and reduced low-density lipoprotein peroxidation rate in vitro. However, we observed an imbalance between oxidizable substrates and antioxidants with an increased lipid peroxidation, whereas the content of reduced glutathione and beta carotene decreased without any variation in vitamin E. Association of antioxidants with n-3 PUFA could prevent lipid peroxidation and enhance the antiatherogenic effects of n-3 polyunsaturated fatty acids.

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Alterations of HDL cholesterol distribution induced by incubation of human serum

Cited by 62 publications

References 17 publications

Apolipoprotein A-I-containing lipoproteins, with or without apolipoprotein A-II, as progenitors of pre-.beta. high-density lipoprotein particles

Apolipoprotein A-I-containing lipoproteins, with or without apolipoprotein A-II, as progenitors of pre-.beta. high-density lipoprotein particles

Low birth weight at term impairs cord serum lipoprotein compositions and concentrations

Effects of fish oil fatty acids on plasma lipids and lipoproteins and oxidant-antioxidant imbalance in healthy subjects

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