Atherogenic changes in low-density lipoprotein particle profiles were not observed in non-obese women with polycystic ovary syndrome

Abstract

Is a preponderance of small dense low-density lipoprotein-cholesterol (LDL-C) observed in non-obese women with polycystic ovary syndrome (PCOS)? Non-obese Korean women with PCOS have no quantitative or qualitative changes in LDL-C profiles. Small dense LDL particles (sd-LDL) are more atherogenic than large buoyant ones and are strongly associated with coronary artery disease independent of other risk factors. Many investigators have found an increased proportion of atherogenic sd-LDL or a decreased mean LDL particle size in women with PCOS, but all of these studies have been based primarily on obese or overweight women with PCOS. This was a casecontrol study evaluating complete lipid and lipoprotein profiles in 64 PCOS patients and 64 age- and BMI-matched controls. All women with PCOS in our study population were not obese. To determine the differences in the LDL particle profiles between PCOS phenotypes, the patients with PCOS were divided into two subgroups according to the presence of clinical or biochemical hyperandrogenism. Using the Rotterdam criteria,we recruited 64 women (1840 years) with PCOS who were attending a tertiary university hospital. A total of 64 premenopausal control women were matched with patients based on exact age and BMI (1.0 kg/m(2)). All the participants fell within the non-obese range of the BMI (25 kg/m(2)) according to the definition of obesity for Asians. The LDL subfraction was analyzed by 3 polyacrylamide gel tube electrophoresis. Seven LDL subclasses were quantified and LDL subclasses 37 were small LDL subfractions. LDL subfraction scores were calculated based on the following weighted scoring system developed by the manufacturer: scores of 5.5 were categorized as phenotype A (large, buoyant LDLs), and those 5.5 were categorized as non-A phenotype (sd-LDLs). The system also determined the mean LDL particle size diameter. There were no differences in the absolute level of LDL-C, mean LDL diameter or percentage of atherogenic sd-LDLs between PCOS patients and controls or between hyperandrogenic and non-hyperandrogenic PCOS subgroups. Also, none of the subjects showed a non-A LDL phenotype. The most notable finding of our study was the difference in the lipoprotein (a) levels and prevalence of its elevation in PCOS patients versus controls (P 0.002 and P 0.004, respectively), and between PCOS subgroups (P 0.030 and P 0.047, respectively). Inclusion of only non-obese subjects, small sample size and lack of information on other potential confounding factors, such as differences in diet and/or exercise patterns. Although our findings suggest that non-obese women with PCOS have no significant quantitative or qualitative changes in LDL-C profile, data on obese Korean women with PCOS could offer complementary findings about the possible relationship between the magnitude of obesity and LDL phenotype. Further investigations are needed to determine whether a change in lipoprotein (a) in non-obese women with PCOS is also found in other ethnic groups. No conflict of interest exists. This study was supported by a grant of the Korean Health Technology RD Project, Ministry of Health Welfare, Republic of Korea (A100624). N/A.