Differential effect of ultracentrifugation on apolipoprotein A-I-containing lipoprotein subpopulations.

Cheung, Marian C.; Wolf, Anitra C.

doi:10.1016/s0022-2275(20)38558-8

Journal of Lipid Research

1988

DOI: 10.1016/s0022-2275(20)38558-8

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Differential effect of ultracentrifugation on apolipoprotein A-I-containing lipoprotein subpopulations.

Marian C. Cheung

Anitra C. Wolf

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Cited by 60 publications

(2 citation statements)

References 31 publications

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“…The historical classification of HDL has been based on ultracentrifugation that resolves two major classes: HDL 2 and HDL 3 (9,10). However this technique has been shown to bring about the decomposition and loss of some native molecular species of HDL (11,12). A newer and less disruptive method of isolation is immunoaffinity chromatography, capable of separating lipoproteins on the basis of differences in apolipoprotein content (12,13).…”

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“…However this technique has been shown to bring about the decomposition and loss of some native molecular species of HDL (11,12). A newer and less disruptive method of isolation is immunoaffinity chromatography, capable of separating lipoproteins on the basis of differences in apolipoprotein content (12,13). This technique has been used to study two major classes of apolipoprotein A-I (apoA-I)-containing lipoproteins: particles containing apoA-I without apoA-II [Lp(A-I)] or particles containing apoA-I and apoA-II [Lp(A-I:A-II)] (14)(15)(16)(17).…”

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Plasma apolipoprotein L concentrations correlate with plasma triglycerides and cholesterol levels in normolipidemic, hyperlipidemic, and diabetic subjects

Duchâteau

Movsesyan

Yamashita

et al. 2000

Journal of Lipid Research

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Apolipoprotein L is a newly recognized component of human plasma lipoproteins. Mainly associated with apoA-I-containing lipoproteins, it is a marker of distinct HDL subpopulations. In an effort to gain inference as to its as yet unknown function, we studied biological determinants of apoL levels in human plasma. The distribution of apoL in normal subjects is asymmetric, with marked skewing toward higher values. No difference was found in apoL concentrations between males and females, but we observed an elevation of apoL in primary hypercholesterolemia (10.1 vs. 8.5 g/mL in control), in endogenous hypertriglyceridemia (13.8 g/mL, P Ͻ 0.001), combined hyperlipidemia phenotype (18.7 g/mL, P Ͻ 0.0001), and in patients with type II diabetes (16.2 g/mL, P Ͻ 0.02) who were hyperlipidemic. Significant positive correlations were observed between apoL and the log of plasma triglycerides in normolipidemia (0.446, P Ͻ 0.0001), endogenous hypertriglyceridemia (0.435, P Ͻ 0.01), primary hypercholesterolemia (0.66, P Ͻ 0.02), combined hyperlipidemia (0.396, P Ͻ 0.04), hypoalphalipoproteinemia (0.701, P Ͻ 0.005), and type II diabetes with hyperlipidemia (0.602, P Ͻ 0.01). Apolipoprotein L levels were also correlated with total cholesterol in normolipidemia (0.257, P Ͻ 0.004), endogenous hypertriglyceridemia (0.446, P ‫؍‬ 0.001), and non-insulin-dependent diabetes mellitus (NIDDM) (0.548, P Ͻ 0.02). No significant correlation was found between apoL and body mass index, age, sex, HDL-cholesterol or fasting glucose and glycohemoglobin levels. ApoL levels in plasma of patients with primary cholesteryl ester transfer protein deficiency significantly increased (7.1 ؎ 0.5 vs. 5.47 ؎ 0.27, P Ͻ 0.006).

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mentioning

confidence: 99%

mentioning

confidence: 99%

Plasma apolipoprotein L concentrations correlate with plasma triglycerides and cholesterol levels in normolipidemic, hyperlipidemic, and diabetic subjects

Duchâteau

Movsesyan

Yamashita

et al. 2000

Journal of Lipid Research

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Understanding and Treating Dyslipidemia Associated With Noninsulin‐Dependent Diabetes Mellitus and Hypertension

McKenney

1993

Pharmacotherapy

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Hypertension and diabetes appear to increase coronary heart disease risk in part by causing an abnormality in lipid metabolism. Most affected are patients with familial dyslipidemic hypertension (FDH) and noninsulin‐dependent diabetes mellitus (NIDDM). The lipid disorders most often encountered in these patients are increased levels of triglycerides, very low‐density lipoprotein (VLDL) cholesterol, and small, dense low‐density lipoprotein (LDL) cholesterol, and low levels of high‐density lipoprotein (HDL) cholesterol. These abnormalities appear to result from increased hepatic secretion of VLDL particles due to increased concentrations of free fatty acids and glucose, reduced VLDL clearance due to reduced activity of lipoprotein lipase, and reduced LDL clearance due to glycosylation of ligand proteins. Treatment of the dyslipidemia associated with FDH should follow the guidelines from the National Cholesterol Education Program. Treatment in men and women with NIDDM should be considered when LDL cholesterol levels are 130 mg/dl or above, triglyceride levels are 200 mg/dl or above, or non‐HDL cholesterol levels are 160 mg/dl or greater. Aggressive lifestyle changes should be initiated first, including weight loss in obese patients, control of glucose levels in those with NIDDM, avoidance of antihypertensive drugs that may worsen lipid levels in patients with FDH, and eating a diet restricting saturated fat and cholesterol. Addition of lipid‐altering drugs should be considered if such changes do not achieve effective lipid control. The agent should be tailored to the patient's lipid profile, in general by using bile acid resins, niacin, or reductase inhibitors to lower LDL cholesterol and gemfibrozil or niacin to lower triglycerides. Niacin should be avoided in patients with NIDDM.

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Metabolism of HDL apolipoprotein A-I and A-II in Type 1 (insulin-dependent) diabetes mellitus

et al. 1992

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Concentrations of HDL cholesterol and apolipoprotein A-I are commonly increased in Type 1 (insulin-dependent) diabetes mellitus but the mechanisms whereby diabetes influences HDL metabolism have not been studied. We investigated the metabolism of HDL apoproteins A-I and II in normolipidaemic Type 1 diabetic men (n = 17, HbA1 6.4-11.9%) without microalbuminuria but with a wide range of HDL cholesterol (0.85-2.10 mmol/l) and in nondiabetic men (n = 18) matched for body mass index and the range of HDL cholesterol. Input rates and fractional catabolic rates for apolipoproteins A-I and II were determined following injection of 125I-apolipoprotein A-I and 131I-apolipoprotein A-II tracers. Additional multicompartmental analysis was performed using a model to describe the kinetics of HDL particles containing only apolipoprotein A-I (Lp A-I) and apolipoprotein A-I and apolipoprotein A-II (Lp A-I/A-II). No gross differences from normal subjects were observed in the mean levels of lipids, lipoproteins, apoproteins and the lipolytic enzymes in the diabetic men as a result of the selection process. Furthermore, the relationship between apolipoprotein A kinetics and plasma HDL cholesterol levels appeared to be preserved in the diabetic group. However, some normal interrelationships were disrupted in the diabetic men. Firstly, the rate of apolipoprotein A-II synthesis was 22% lower than in control subjects (p less than 0.05). Modelling indicated that this was due to decreased input of Lp A-I/A-II particles whereas the input of Lp A-I particles was similar in the two groups. Secondly, there was no correlation between VLDL triglyceride and HDL cholesterol or VLDL triglyceride and the fractional catabolic rate of apolipoproteins A-I and A-II in diabetic men in contrast to that seen in control subjects. We conclude that there is a disruption in the normal association between VLDL and HDL metabolism in Type 1 diabetic men and postulate that the observed differences may be due to the therapeutic use of exogenous insulin.

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Differential effect of ultracentrifugation on apolipoprotein A-I-containing lipoprotein subpopulations.

Cited by 60 publications

References 31 publications

Plasma apolipoprotein L concentrations correlate with plasma triglycerides and cholesterol levels in normolipidemic, hyperlipidemic, and diabetic subjects

Plasma apolipoprotein L concentrations correlate with plasma triglycerides and cholesterol levels in normolipidemic, hyperlipidemic, and diabetic subjects

Understanding and Treating Dyslipidemia Associated With Noninsulin‐Dependent Diabetes Mellitus and Hypertension

Metabolism of HDL apolipoprotein A-I and A-II in Type 1 (insulin-dependent) diabetes mellitus

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