Apolipoprotein E in High-Density Lipoprotein in Patients with Old Cerebral Infarction

• Published in: Nihon Rōnen Igakkai zasshi Vol. 24; no. 6; pp. 561 - 566
• Main Authors: Toratani, Yoshiyuki, Ikeda, Hiroshi, Sakamoto, Kenichi, Shimizu, Eiji, Maeda, Jiro
• Format: Journal Article
• Language: Japanese
• Published: Japan The Japan Geriatrics Society 01.11.1987
• Subjects: Aged; Apolipoproteins E - blood; Arteriosclerosis - diagnosis; cerebral infarction; Cerebral Infarction - blood; Female; HDL-E ratio; HDL-with apo E; Humans; Lipoproteins, HDL - blood; Male; Middle Aged; negative-atherogenic index; Risk Factors
• ISSN: 0300-9173
• DOI: 10.3143/geriatrics.24.561

Mahley et al had proposed that HDL-with apo E would play important roles in protective or anti-atherosclerotic functions of HDL, that is, in reverse cholesterol transporting to liver from peripheral tissues and in competing with LDL for binding to LDL-receptors. And Bittolo Bon et al. in 1984 reported for the first time that apo E concentration in HDL in survivors of myocardial infarction was significantly lower than that in controls. But apo E in HDL (HDL-E) in patients with old cerebral infarction (OCI) as the atherosclerotic subjects was not yet determined. So, in order to estimate whether HDL-E could be clinically expected to be one of the anti-atherogenic index, HDL-E in OCI was determined in this study by Ikeda's method using quantitative immunofixation electrophoresis, by which HDL-E was detected for the first time at near the α2-globulin region behind α lipoprotein (that is, HDL-without apo E). Samples were sera acquired in fasting from normolipidemic, aged 50-70 years old, 10 male and 10 female OCI without hepatobiliary disorders and age-matched healthy controls, and were examined as to triglycedies, cholesterol, apo A-I, apo B and apo E, in addition to determination of HDL-E. Cholesterol in HDL (HDL-C) and apo A-I were lower, and apo B, apo B/apo A-I ratio (B/A-I) and atherogenic index (A.I.) [(cholesterol-HDL-C)/HDL-C] were significantly higher in OCI than in controls. No significant difference in serum levels of apo E between two groups was observed, but HDL-E concentrations (0.6±0.2vs 1.4±0.3mg/dl, p<0.001), HDL-E ratios (HDL-E×100/serum apo E, %) (16.8±7.2 vs 42.1±6.4%, p<0.001), ratios of HDL-E/apo A-I (0.5±0.2 vs 1.1± 0.2%, p<0.001) and ratios of HDL-E/HDL-C (1.9±0.7 vs 2.8±0.6%, p<0.001) were significantly lower in OCI than in controls. Therefore, this result would reveal the disturbance of distribution of apo E to HDL in atherosclerotic subjects as OCI. In other words, it would be suggested from this result that anti-atherosclerotic functions of HDL in which apo E abnormally decreased would be weakened, as well as Bittolo Bon's speculation. And, as new information the significant reverse correlation between HDL-E ratios and levels of apo B which was main apolipoprotein of LDL was recognized in this study, so the information would clear the suspicion that HDL-with apo E might induce to be atherogenic hyper-low-density lipoproteinemia because of competing with LDL for natural binding to receptors. And more, HDL-E ratios significantly correlated with negative-atherogenic parameters of HDL-C and apo A-I, and inversely correlated with atherogenic parameters of B/A-I and A.I.. The results in this paper suggest that HDL-E ratio would be able to be evaluated as a negative-atherogenic index.