ISOFORM PATTERNS OF APOLIPOPROTEIN-E IN DIABETES-MELLITUS

被引：17

作者：

BLACK, SC ^{[1
]}

HEWETT, S ^{[1
]}

KOTUBI, Y ^{[1
]}

BRUNT, RV ^{[1
]}

RECKLESS, JPD ^{[1
]}

机构：

[1] ROYAL UNITED HOSP,BATH INST CLIN SCI,DIABET & LIPID RES LAB,COMBE PK,BATH BA1 3NG,ENGLAND

来源：

DIABETIC MEDICINE | 1990年 / 7卷 / 06期

关键词：

Apolipoprotein E isoforms; Apolipoproteins; Diabetes mellitus; Glycosylation; Hyperlipidaemia; Very low density lipoproteins;

D O I：

10.1111/j.1464-5491.1990.tb01437.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Apolipoproteins in delipidated VLDL preparations from normal, diabetic, and non‐diabetic hyperlipidaemic subjects were analysed by SDS‐polyacrylamide gel electrophoresis, and by isoelectric focusing. On electrophoresis, diabetic VLDL contained more apolipoprotein E (17.3 ± 7.3 (± SD)%, n = 54) than did VLDL from hyperlipidaemic (13.4 ± 4.2%, n = 52; p < 0.005) or normal (12.4 ± 2.6%, n = 29; p < 0.001) subjects. Apolipoprotein E excess was also seen when subgroups were characterized by apolipoprotein E phenotype. In diabetic patients of E3/E3 phenotype, apolipoprotein E was 16.4 ± 6.0% (n = 25), compared with 12.9 ± 2.5% in control subjects (n = 14; p = 0.008). Acidic isoforms were more common in 44 diabetic patients with E3/E3 phenotype; E3, E2, E1, and E1′ as percentage of total E apolipoprotein were 58.3 ± 7.6, 24.5 ± 4.4, 13.7 ± 4.5, and 3.8 ± 4.3% respectively, compared with 63.5 ± 10.4 (p = 0.034), 19.1 ± 5.3 (p < 0.001), 13.7 ± 6.5 (NS), and 3.7 ± 2.1% (NS) in 21 normal subjects. In 31 diabetic patients, of apolipoprotein E3/E3 phenotype, E3, E2, E1 and E1′ were 60.2 ± 7.3, 23.4 ± 9.4, 11.1 ± 4.1, and 5.4 ± 3.7%, respectively, compared with 68.0 ± 7.1 (p < 0.001), 21.9 ± 6.4 (NS), 6.3 ± 3.9 (p < 0.001), and 3.7 ± 2.5 (p < 0.05)% in 32 hyperlipidaemic patients. Diabetic patients of E3/E2 phenotype showed less apolipoprotein E3 than normal or hyperlipidaemic subjects, with a similar trend for apolipoprotein E4 in those of E4/E3 phenotype. Increases in minor apolipoprotein E isoforms imply more post‐translational protein modification in people with diabetes. 1990 Diabetes UK

引用

页码：532 / 539

页数：8

共 43 条

[11]

Mahley RW, Angelin B., Type III hyperlipoproteinaemia: recent insights into the genetic defect of familial dysbetalipoproteinaemia, Adv Intern Med, 29, pp. 385-411, (1984)

[12]

Mahley RW, Innerarity TL, Rall SC, Weisgraber KH, Plasma lipoproteins: apolipoprotein structure and function, J Lipid Res, 25, pp. 1277-1294, (1984)

[13]

Weisgraber KH, Innerarity TL, Mahley RW, Role of the lysine residues of plasma lipoproteins in high affinity binding to cell surface receptors on human fibroblasts, J Biol Chem, 253, pp. 9053-9062, (1978)

[14]

Mahley RW, Innerarity TL, Pitas RE, Weisgraber KH, Brown JH, Gross E., Inhibition of lipoprotein binding to cell surface receptors of fibroblasts following selective modification of arginyl residues in arginine‐rich and B apoproteins, J Biol Chem, 252, pp. 7279-7287, (1977)

[15]

Weisweiler P., Jungst D., Schwandt P., Quantitation of apolipoprotein E isoforms in diabetes mellitus, Horm Metab Res, 15, pp. 201-205, (1983)

[16]

Kannel WB, McGee DL, Diabetes and glucose tolerance as risk factors for cardiovascular disease: The Framingham Study, Diabetes Care, 2, pp. 120-126, (1979)

[17]

Jarrett RJ, Keen H., Chakrabarti R., Diabetes, hyperglycaemia and arterial disease, Complications of Diabetes, pp. 179-203, (1982)

[18]

Waller BF, Palumbo PJ, Lie JT, Roberts WC, Status of the coronary arteries at necropsy in diabetes mellitus with onset after age 30 years, Am J Med, 69, pp. 498-506, (1980)

[19]

Kissebah AH, Alfarsi S., Evans DJ, Adams PW, Plasma low density lipoprotein kinetics in non‐insulin dependent diabetes mellitus, J Clin Invest, 71, pp. 655-667, (1983)

[20]

Betteridge DJ, Lipoprotein metabolism, Recent Advances in Diabetes, 2, pp. 91-107, (1986)

← 1 2 3 4 5 →