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Hypothesis/Aims of study. Dyslipidemia is a common metabolic disorder and is an atherogenic factor in the development of cardiovascular disease in women with polycystic ovary syndrome. Currently, four phenotypes of polycystic ovary syndrome are distinguished, associated in varying degrees of severity with dyslipidemia, insulin resistance, impaired glucose tolerance, and diabetes mellitus on one hand and chronic inflammation and oxidative stress on the other. Hyperandrogenic phenotypes (A, B, C) in polycystic ovary syndrome are associated with the development of adverse metabolic disorders and associated complications. The aim of this study was to evaluate the lipid profile in the serum of women of reproductive age with various polycystic ovary syndrome phenotypes. Study design, materials and methods. The study included 86 women of reproductive age from 22 to 37 years old (average age was 26.6 4.3 years), who, in accordance with polycystic ovary syndrome phenotypes (A, B, C, D), were divided into four groups. We studied the levels of anti-Mllerian hormone, follicle-stimulating and luteinizing hormones, prolactin, estradiol, and androgens from days 2 to 5 of the menstrual cycle. The levels of progesterone in the blood serum were determined by the enzyme immunoassay on days 20 to 23 of the menstrual cycle for three consecutive cycles. We also used echographic methods for diagnosing polycystic ovaries. All women underwent a biochemical blood test with an assessment of the lipid profile parameters (total cholesterol, triglycerides, high-density lipoproteins (HDL), and low-density lipoproteins, LDL). Besides, an oral glucose tolerance test was assessed with the study of plasma glucose and insulin levels on an empty stomach and two hours after ingestion of 75 g of glucose, the HOMA-IR index being used to assess insulin resistance. Results. Phenotype A was found in 40 (46.5%) women with polycystic ovary syndrome, phenotype B in 22 (25.6%), phenotype C in 10 (11.6%), and phenotype D (non-androgenic) in 14 (16.3%) patients with PCOS. Of those 42 (48.8%) individuals had changes in carbohydrate metabolism (impaired glucose tolerance), of whom 39 (92.8%) women had androgenic polycystic ovary syndrome phenotypes (A, B, C). Both non-androgenic phenotype D and impaired glucose tolerance were found in 7.2% of cases. In women with hyperandrogenic polycystic ovary syndrome phenotypes, both the fasting and stimulated insulin levels were increased significantly comparing to the non-androgenic anovulatory phenotype (p 0.05). The HOMA-IR index in women with phenotypes A, B and C was significantly (p 0.05) higher than in patients with non-androgenic phenotype D. When evaluating the lipid profile parameters, no significant differences in cholesterol level and atherogenic coefficient in women with various polycystic ovary syndrome phenotypes were found. The levels of triglycerides and LDL were significantly (p 0.05) higher in women with androgenic phenotype B compared to those in patients with non-androgenic phenotype D and they correlated significantly (p 0.05) with the serum levels of androgens and sex hormone-binding globulin (SHBG). Patients with androgenic polycystic ovary syndrome phenotypes (A and B) had significantly (p 0.05) decreased HDL levels that correlated negatively (r = 0.29; p 0.05) with the levels of free testosterone and SHBG, when compared to the same parameters in women with non-androgenic phenotype D. In women with androgenic polycystic ovary syndrome phenotypes (A, B, C), a significant correlation (r = 0.27; p 0.05) between the levels of stimulated insulin and SHBG were found, and a direct relation (r = 0.32; p 0.05) between those parameters and increased levels of triglycerides and LDL was also revealed. Conclusion. In women with hyperandrogenic and anovulatory polycystic ovary syndrome phenotypes A and B, atherogenic dyslipidemia and impaired carbohydrate metabolism were significantly more pronounced, when compared with patients with non-androgenic phenotype D. A differential and personalized approach to the examination of patients with various polycystic ovary syndrome phenotypes is an important step in the prevention of the risks of developing cardiovascular diseases in women of reproductive age.

The main ideas about the pathogenesis of ovarian dysfunction in women with diabetes mellitus (DM) type 1 are presented. The role of increased opioid and dopaminergic tone in the pathogenesis of reducing the synthesis of the gonadotropin-releasing hormone by the hypothalamus in women with type 1 diabetes was analyzed. Presented the data of relationship between ovarian hormonal insufficiency in women with type 1 diabetes with possible damage of positive feedback mechanism of the ovaries and the pituitary gland, which intactness is necessary for the maturation of the dominant follicle and ovulation. The results of studies, suggested that the high doses of exogenously administered insulin in type 1 DM lead to stimulation of androgen synthesis in teca cells and ovarian stroma and the development of ovarian  hyperandrogenemia, as well as polycystic ovary syndrome, are reduced. In addition to exogenous hyperinsulinemia, in the pathogenesis of ovarian dysfunction, the value of the deficiency of endogenous insulin, leading to a violation of steroidogenesis in the tissues of the ovary and anovulation, is proved. The role of insulin deficiency and hyperglycemia in the development of metabolic stress lead to ovarian dysfunction in patients with type 1 diabetes was analyzed.