Abstract
Objective:Insulin resistance (IR) seems to be the main pathogenic factor in polycystic ovary syndrome (PCOS). Adiponectin and tumor necrosis factor-alpha (TNF-α) are important in IR. The aim of this study was to evaluate the correlations of osteocalcin, adiponectin, and TNF-α with IR in PCOS.Materials and Methods:A total of 60 women were divided into two groups. The first group constituted 44 patients with PCOS and the control group comprised 16 healthy women. Osteocalcin, adiponectin, TNF-α levels, body mass index (BMI), and IR in the fasting state were assessed and correlations of these parameters were evaluated.Results:Homeostasis model assessment (HOMA)-IR, adiponectin, osteocalcin, and androstenedione levels were significantly increased in the PCOS group. A moderate positive correlation between BMI and HOMA-IR, a moderate negative correlation between TNF-α and osteocalcin, and a mild negative correlation between adiponectin and BMI were detected in PCOS.Conclusion:Osteocalcin may have impact on adiponectin, TNF-α, and IR levels in PCOS. Different osteocalcin levels in patients with PCOS may be responsible for explaining PCOS heterogeneity.
Highlights
Polycystic ovary syndrome (PCOS) is a common and heterogeneous disease characterized by anovulation, hyperandrogenism, and/or polycystic ovaries[1,2]
Homeostasis model assessment (HOMA)-Insulin resistance (IR), adiponectin, osteocalcin, and androstenedione levels were significantly increased in the polycystic ovary syndrome (PCOS) group
We aimed to evaluate the correlations of blood osteocalcin, adiponectin, and tumor necrosis factor (TNF)-α levels with IR in PCOS
Summary
Polycystic ovary syndrome (PCOS) is a common and heterogeneous disease characterized by anovulation, hyperandrogenism, and/or polycystic ovaries[1,2]. An important consideration is whether such adipocytokines as adiponectin, a potential mediator of insulin resistance (IR), are implicated in the pathogenesis of PCOS[3]. An abundant adipocyte-derived cytokine, are strongly correlated with measures of IR[4,5]. Gonzalez et al[6] illustrated that hyperglycemia caused an increase in reactive oxygen species (ROS) generation from peripheral blood mononuclear cells (MNC). Increased TNF release from MNC in response to hyperglycemia may be an underlying mechanism for IR in PCOS. Previous animal studies showed that osteocalcin stimulated the expression of insulin in islets and of adiponectin in adipocytes with increased insulin secretion and sensitivity[9]. We aimed to evaluate the correlations of blood osteocalcin, adiponectin, and TNF-α levels with IR in PCOS. We evaluated the relationship of these with some hormonal parameters
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