Quantitation of apolipoprotein A-I of human plasma high density lipoprotein
High density lipoproteins (HDL) may be controlled via their major apolipoprotein, A-I. To study this apolipoprotein, a simple, precise, and accurate immunodiffusion assay for A-I was developed and applied in a sample of Bell Telephone Company employees. A-I showed a slight increase with age in men (...
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Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 1976-06, Vol.25 (6), p.633-644 |
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Zusammenfassung: | High density lipoproteins (HDL) may be controlled via their major apolipoprotein, A-I. To study this apolipoprotein, a simple, precise, and accurate immunodiffusion assay for A-I was developed and applied in a sample of Bell Telephone Company employees. A-I showed a slight increase with age in men (
r = 0.11,
n = 263) and women (
r = 0.15,
n = 257). A-I correlated closely with HDL cholesterol (
r = 0.72). It was weakly related to total triglyceride in women (
r = 0.24) but was inversely related in men (
r = −0.17). Women on estrogen had the highest A-I levels (149 mg/dl ± 26,
x
± S.D.,
n = 29,
p < 0.05), followed by women on combination oral contraceptives (141 ± 26,
n = 80) whereas women on no medication had lower levels (129 ± 25,
n = 99,
p < 0.01) but men had the lowest levels (120 ± 20,
p < 0.01). In a separate group of 14 women given estrogen for 2 wk (1 μg/kg/day), A-I increased by 24%. Thus A-I is increased by exogenous and, most likely, endogenous estrogen. Among hyperlipidemic referral subjects, those with hypercholesterolemia (
n = 43) and hypertriglyceridemic women (
n = 33) had normal A-I levels. Among hypertriglyceridemic men both A-I and HDL cholesterol values were decreased (115 ± 20,
p < 0.01 and 37 ± 3,
p < 0.01, respectively,
n = 68) but were significantly lower among a group of myocardial infarction survivors (107 ± 16,
p < 0.01, and 27 ± 6,
p < 0.01, respectively,
n = 24). High density lipoprotein levels and the content of cholesterol in HDL associated with A-I appear to be decreased in coronary heart disease. |
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ISSN: | 0026-0495 1532-8600 |
DOI: | 10.1016/0026-0495(76)90060-3 |