Susceptibility of small, dense, low-density lipoproteins to oxidative modification in subjects with the atherogenic lipoprotein phenotype, pattern B

Abstract Context: An altered lipid profile is common in polycystic ovary syndrome (PCOS) and is usually characterized by increased triglycerides and low high-density lipoprotein (HDL)-cholesterol levels. In the general population, these alterations are often associated with the increase of small low-density lipoproteins (LDLs) in the so-called “atherogenic lipoprotein phenotype” (ALP) that determines a further increase of cardiovascular risk. In this study, we evaluated the presence of ALP in the plasma of women with PCOS. Setting: Measurements and analysis of LDL size were performed at the Clinic of Endocrinology, Diabetes, and Clinical Nutrition, University Hospital, Zurich. PCOS patients were recruited at the Department of Clinical Medicine, University of Palermo, and the Department of Obstetrics and Gynecology, University of Pisa. Patients: Thirty patients with PCOS (hyperandrogenism and chronic anovulation) and 24 matched controls were studied. Anthropometric data, blood glucose, serum insulin lipid profile, and LDL size and subclasses were evaluated. Results: Compared with controls, patients with PCOS had higher plasma concentrations of insulin and triglycerides and lower HDL-cholesterol concentrations but no differences in LDL-cholesterol and total cholesterol. Patients with PCOS had smaller LDL size due to a reduction in LDL subclass I, with a concomitant increase in LDL subclasses III and IV. Fourteen PCOS patients had an increase of smaller LDL particles, and it represented the second most common lipid alteration after decrease in HDL-cholesterol. However, because in this PCOS population hypertriglyceridemia was only present in two patients, complete ALP was relatively uncommon. Conclusions: Increase of type III or type IV LDL subclasses is a common finding in PCOS and represents the second most common lipid alteration after HDL-cholesterol decrease. However, in our PCOS patients, because of relatively low triglyceride levels, complete ALP is uncommon.

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Inter-relationships between small, dense low-density lipoprotein (LDL), plasma triacylglycerol and LDL apoprotein B in an atherogenic lipoprotein phenotype in free-living subjects

Clinical Science ◽

10.1042/cs19990056 ◽

1999 ◽

Vol 97 (3) ◽

pp. 269 ◽

Cited By ~ 12

Author(s):

B.A. GRIFFIN ◽

A.M. MINIHANE ◽

N. FURLONGER ◽

C. CHAPMAN ◽

M. MURPHY ◽

...

Keyword(s):

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Low Density ◽

Free Living ◽

Atherogenic Lipoprotein ◽

Apoprotein B ◽

Plasma Triacylglycerol ◽

Atherogenic Lipoprotein Phenotype ◽

Lipoprotein Phenotype

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Comparative Effects of Cerivastatin and Fenofibrate on the Atherogenic Lipoprotein Phenotype in Proteinuric Renal Disease

Journal of the American Society of Nephrology ◽

10.1681/asn.v122341 ◽

2001 ◽

Vol 12 (2) ◽

pp. 341-348

Author(s):

CHRISTOPHER J. DEIGHAN ◽

MURIEL J. CASLAKE ◽

MICHAEL MCCONNELL ◽

J. MICHAEL BOULTON-JONES ◽

CHRISTOPHER J. PACKARD

Keyword(s):

Low Density Lipoprotein ◽

Density Lipoprotein ◽

High Density Lipoproteins ◽

Low Density ◽

Atherogenic Lipoprotein ◽

Fenofibrate Treatment ◽

Remnant Lipoproteins ◽

Atherogenic Lipoprotein Phenotype ◽

Nephrotic Range Proteinuria ◽

Lipoprotein Phenotype

Abstract. Patients with nephrotic-range proteinuria have impaired clearance of triglyceride-rich lipoproteins. This results in the atherogenic lipoprotein phenotype (mild hypertriglyceridemia, low high-density lipoproteins [HDL], and excess small, dense low-density lipoproteins [LDLIII]). Excess remnant lipoproteins (RLP) are linked to hypertriglyceridemia and may contribute to the atherogenicity of nephrotic dyslipidemia. A randomized crossover study compared the effects of a statin (cerivastatin) and a fibrate (fenofibrate) on LDLIII and RLP in 12 patients with nephrotic-range proteinuria. Cerivastatin reduced cholesterol (21%, P < 0.01), triglyceride (14%, P < 0.05), LDL cholesterol (LDL-C; 23%, P < 0.01), total LDL (18%, P < 0.01), and LDLIII concentration (27% P < 0.01). %LDLIII, RLP-C, and RLP triglyceride (RLP-TG) were unchanged. Plasma LDLIII reduction with cerivastatin treatment correlated with LDL-C reduction (r2 = 34%, P < 0.05). Fenofibrate lowered cholesterol (19%), triglyceride (41%), very low-density lipoprotein cholesterol (52%), LDLIII concentration (49%), RLP-C (35%), and RLP-TG (44%; all P < 0.01). Fenofibrate also reduced %LDLIII from 60 to 33% (P < 0.01). HDL-C (19%, P < 0.01) increased with fenofibrate treatment; LDL-C and total LDL were unchanged. The reduction in LDLIII concentration and RLP-C with fenofibrate treatment correlated with plasma triglyceride reduction (LDLIII r2 = 67%, P < 0.001; RLP cholesterol r2 = 58%, P < 0.005). Serum creatinine increased with fenofibrate treatment (14%, P < 0.01); however, creatinine clearance was unchanged. LDLIII concentration was 187 ± 85 mg/dl after cerivastatin treatment and 133 ± 95 mg/dl after fenofibrate treatment. Cerivastatin and fenofibrate reduce LDLIII concentration in nephrotic-range proteinuria. However, atherogenic concentrations of LDLIII remain prevalent after either treatment. Fenofibrate but not cerivastatin reduces remnant lipoproteins. The two treatments seem to reduce LDLIII by different mechanisms, suggesting a potential role for combination therapy to optimize lowering of LDLIII and RLP.

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