Endocrine Abstracts

The polycystic ovary syndrome (PCOS) is associated with features of the insulin resistance syndrome and altered glucose homeostasis. Factors that play an important role in these processes are still emerging. Adipokines and pro-inflammatory cytokines may be involved in development of insulin resistance in PCOS. The purpose of this study was to determine if a relationship exists between adiponectin, resistin, leptin, interleukin (IL) 4, IL6, IL10, tumor necrosis factor α (TNF α) and insulin resistance indices in lean women with PCOS.

Methods: Fasting insulin, glucose, C-peptide, lipid profile, FSH, LH, prolactin, testosterone, sex hormone binding globulin, 17-hydroxyprogesterone, adiponectin, resistin, leptin, IL4, IL6, IL10, TNF α serum concentrations were analyzed at basal conditions in 12 lean women with PCOS (BMI<25 kg/m²) and 17 age- and weight-matched healthy controls. Oral glucose tolerance test was performed. Homeostasis model assessment insulin resistance (HOMA-IR), Matsuda and Cederholm index were calculated. Statistics: Mann–Whitney U test and Spearman correlation.

Results: Matsuda and Cederholm index were significantly lower in lean women with PCOS than in control group (P<0.05 for both). Fasting glucose, insulin, C-peptide and HOMA-IR did not differ between groups. Adiponectin tended to be lower in PCOS (P<0.054). Resistin was significantly lower in PCOS than in control group (P<0.05). Leptin, IL4, IL6, IL10, TNF α levels did not differ between groups. In women with PCOS i) IL4 correlated significantly negatively with fasting glucose (P<0.01), ii) leptin correlated significantly positively with LDL cholesterol (P<0.05) and significantly negatively with Matsuda index (P<0.05).

Conclusions: In lean women with PCOS, the insulin sensitivity was decreased, however, serum levels of resistin were lower than in control group, leptin levels were associated with markers of insulin resistance and IL4 was connected with fasting blood glucose. Supported with the grants NS/9839-4 and CZ.2.17/1.1.00/32386.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.