Parental history of early myocardial infarction is associated with decreased levels of lipoparticle AI in adolescents.

Amouyel, Philippe; Isorez, Dominique; Bard, Jean‐Marie; Goldman, Marc; Lebel, P.; Zylberberg, G.; Fruchart, Jean‐Charles

doi:10.1161/01.atv.13.11.1640

Cited by 39 publications

(14 citation statements)

References 25 publications

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“…Previously, it was shown that transgenic mice producing human apo A-I have significantly less atherosclerosis than those producing both apo A-I and apo A-II when fed an atherogenic diet [18,24,25]. Clinical studies have indicated that the increased levels of LP A-I particles are associated negatively with the degree of arteriographically defined coronary disease [26,27]. Premenopausal women have higher levels of LP A-I, suggesting that this may have beneficial effect in reducing cardiovascular risk in these subjects [28].…”

Section: Discussionmentioning

confidence: 99%

Rosuvastatin selectively stimulates apolipoprotein A-I but not apolipoprotein A-II synthesis in Hep G2 cells

et al. 2008

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Section: Discussionmentioning

confidence: 99%

Rosuvastatin selectively stimulates apolipoprotein A-I but not apolipoprotein A-II synthesis in Hep G2 cells

et al. 2008

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“…18 Clinical studies have indicated that the increased levels of LP-AI particles are associated negatively with the degree of arteriographically defined coronary disease. 19,20 Premenopausal women have higher levels of LP-AI, suggesting that this may have a beneficial effect in reducing cardiovascular risk in these subjects. 21 Oral estrogen replacement therapy in postmenopausal women was shown to increase LP-AI levels.…”

Section: See Page 1707mentioning

confidence: 99%

Niacin, but Not Gemfibrozil, Selectively Increases LP-AI, a Cardioprotective Subfraction of HDL, in Patients With Low HDL Cholesterol

Sakai

Kamanna

Kashyap

2001

ATVB

108

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Abstract-Evidence indicates that the high density lipoprotein (HDL) subfraction containing apolipoprotein A-I without apolipoprotein AII (LP-AI) is more antiatherogenic than HDL particles containing apolipoprotein A-I and apolipoprotein A-II (LP-AIϩAII). This study examined the effect of extended-release niacin (niacin-ER) and gemfibrozil on LP-AI and LP-AIϩAII particles in patients with low levels of HDL cholesterol (HDL-C). Mechanisms by which these agents modulate HDL particles were investigated by in vitro studies using human hepatoblastoma (Hep G2) cells. A total of 139 patients with low HDL-C (Յ40 mg/dL) were randomized to niacin-ER or gemfibrozil in a multicenter double-blind trial. Patients were dose-escalated with once-nightly niacin-ER (1 to 2 g) or gemfibrozil (1.2 g) for 19 weeks. Niacin-ER had a greater effect in raising HDL-C and apolipoprotein A-I levels than did gemfibrozil. Niacin-ER at 1-and 2-g doses increased LP-AI levels by 8.7Ϯ4.0% (Pϭ0.033) and 24.0Ϯ4.4% (PϽ0.001), respectively. Gemfibrozil had no consistent effect on LP-AI levels. LP-AIϩAII levels increased 5% to 8% by both agents. In vitro studies showed that niacin, but not gemfibrozil, selectively decreased the uptake of 125 I-labeled LP-AI holoparticles by Hep G2 cells. The uptake of [ 3 H]cholesterol ester was Ϸ75% greater from LP-AI versus LP-AIϩAII particles, but neither niacin nor gemfibrozil affected cholesterol ester uptake. These data indicate that unlike gemfibrozil, niacin selectively increases LP-AI compared with LP-AIϩAII particle concentration in patients with low HDL-C levels. The mechanism of action of increased LP-AI concentration appears to be mediated by decreased hepatic removal of LP-AI particles, which are more efficient in reverse cholesterol transport, thus suggesting an additional mechanism by which niacin mediates its antiatherogenic properties.

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“…15,16 However, recent studies indicated decreased levels of both LP A-I and LP A-IϩA-II particles in patients with hypertriglyceridemia, familial combined hyperlipidemia, and a history of coronary heart disease.…”

mentioning

confidence: 99%

“…[12][13][14] LP A-I is also associated negatively with extent of arteriographically defined coronary disease. 15,16 However, recent studies indicated decreased levels of both LP A-I and LP A-IϩA-II particles in patients with hypertriglyceridemia, familial combined hyperlipidemia, and a history of coronary heart disease. 17 In spite of several biological mechanisms proposed to support a beneficial role for estrogen, 18 the favorable alterations in HDL levels appear to be a well-established effect of estrogen in preventing atherosclerotic cardiovascular disease.…”

mentioning

confidence: 99%

Estradiol Stimulates Apolipoprotein A-I– but Not A-II–Containing Particle Synthesis and Secretion by Stimulating mRNA Transcription Rate in Hep G2 Cells

Jin

Kamanna

Kashyap

1998

ATVB

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Abstract-Estrogen therapy increases plasma HDL levels, which may reduce cardiovascular risk in postmenopausal women. The mechanism of action of estrogen in influencing various steps in hepatic HDL and apolipoprotein (apo) A-I synthesis and secretion are not fully understood. In this study, we have used the human hepatoblastoma cell line (Hep G2) as an in vitro model system to delineate the effect of estradiol on multiple regulatory steps involved in hepatic HDL metabolism. Incubation of Hep G2 cells with estradiol resulted in the following statistically significant findings: (1) increased accumulation of apoA-I in the medium without affecting uptake/removal of radiolabeled HDL-protein; (2) accelerated incorporation of [ 3 H]leucine into apoA-I; (3) selective increase in [ 3 H]leucine incorporation into lipoprotein (LP) A-I but not LP A-IϩA-II HDL particles (HDL particles without and with apoA-II, respectively); (4) increased ability of apoA-I-containing particles to efflux cholesterol from fibroblasts; (5) stimulated steady state apoA-I but not apoA-II mRNA expression; and (6) increased newly transcribed apoA-I mRNA message without effect on apoA-I mRNA half-life. The data indicate that estradiol stimulates newly transcribed hepatic apoA-I mRNA, resulting in a selective increase in LP A-I, a subfraction of HDL that is associated with decreased atherosclerotic cardiovascular disease, especially in premenopausal women. (Arterioscler Thromb Vasc Biol. 1998;18:999-1006.) Key Words: estrogen Ⅲ high density lipoproteins Ⅲ apolipoprotein A-I Ⅲ cardiovascular disease A therosclerotic cardiovascular disease is the leading cause of mortality among postmenopausal women. Abnormalities in lipid and lipoprotein metabolism (eg, increased LDL and decreased HDL levels) commonly seen in postmenopausal women have been attributed to the increased coronary heart disease-related mortality in these individuals.1-3 Because the decline in estrogen levels is the primary metabolic alteration observed in postmenopausal women, it has been thought that endogenous concentrations of estrogen may have fundamental roles in lipoprotein-mediated development of atherosclerotic coronary heart disease. Clinical studies have indicated that estrogen therapy significantly elevated plasma HDL levels and decreased LDL concentrations, suggesting a favorable effect on the plasma lipoprotein profile. 4 -6 Recent comparative studies by meta-analysis showed that postmenopausal women on estrogen therapy have a lower relative risk of coronary events than postmenopausal women who are not on estrogen therapy. 7,8 Immunoaffinity techniques have revealed that HDL particles exist in 2 major classes: LP A-I and LP A-IϩA-II (ie, without and with apoA-II, respectively).9 ApoA-I and apoA-II are major proteins of HDL. There is considerable evidence to suggest that LP A-I is more importantly linked to decreased atherosclerosis risk. Premenopausal women have higher levels of LP A-I than age-matched men. 10 Oral estrogen replacement therapy in postmenopausal women was sho...

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Parental history of early myocardial infarction is associated with decreased levels of lipoparticle AI in adolescents.

Cited by 39 publications

References 25 publications

Rosuvastatin selectively stimulates apolipoprotein A-I but not apolipoprotein A-II synthesis in Hep G2 cells

Rosuvastatin selectively stimulates apolipoprotein A-I but not apolipoprotein A-II synthesis in Hep G2 cells

Niacin, but Not Gemfibrozil, Selectively Increases LP-AI, a Cardioprotective Subfraction of HDL, in Patients With Low HDL Cholesterol

Estradiol Stimulates Apolipoprotein A-I– but Not A-II–Containing Particle Synthesis and Secretion by Stimulating mRNA Transcription Rate in Hep G2 Cells

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