Lipoprotein subclasses compensate the classic atherogenic lipid profile of women with polycystic ovary syndrome, but common antiandrogenic treatments worsen their lipidome

Abstract Objectives Patterns of circulating inflammatory glycoproteins and lipoprotein subclasses are not well-defined in polycystic ovary syndrome (PCOS). We aimed to describe these profiles and effects of drug intervention on those parameters. Design Cross-sectional and longitudinal interventional prospective studies. Methods The cross-sectional study included 340 patients with PCOS and 92 non-hyperandrogenic women. Glycoprotein and lipoprotein profiles were measured by proton-nuclear magnetic resonance spectroscopy. We also analyzed their changes after treatment with metformin, an oral contraceptive, or an oral contraceptive plus spironolactone in 13, 20, and 16 women with PCOS, respectively. Results Circulating glycoproteins were increased in obese women, regardless of PCOS. PCOS-associated increased VLDL-cholesterol and VLDL-triglycerides, but reduced HDL-cholesterol, HDL-triglycerides, IDL-triglycerides, LDL-cholesterol, and LDL-triglycerides, compared with controls. Regarding lipoprotein particles (P), PCOS patients had higher large and medium VLDL-P and, accordingly, larger VLDL sizes than controls. Interestingly, women with PCOS also showed larger HDL-P and HDL sizes than controls, a pattern that is not associated with cardiovascular disease. However, large and medium LDL-P were reduced in patients. Circulating glycoproteins increased with all treatments. Antiandrogenic regimens induced a larger increase in HDL-cholesterol, HDL-triglycerides, IDL-triglycerides, IDL-cholesterol, and LDL-triglycerides compared with metformin. Similarly, these regimens induced a larger increase in medium LDL-P, medium HDL-P, and small HDL-P than metformin. Small LDL-P only increased after oral contraceptive plus spironolactone. Conclusions Inflammatory glycoprotein biomarkers are linked to obesity but not to PCOS. PCOS is associated with a classic atherogenic lipid pattern, but a less unfavorable lipoprotein subclass distribution. Antiandrogenic regimens induce negative lipid changes in these women.