AIM: The aim of this study was to investigate the relationship between four circulating adipocytokines (apelin, vaspin, visfatin, adiponectin) and markers of insulin sensitivity, in the context of polycystic ovary syndrome (PCOS) in adolescents. SUBJECTS AND METHODS: 48, obese, adolescent girls (mean age: 15.6±3.4 years, mean body mass index standard deviation score (BMI-SDS): 2.31±0.1), and 37 control subjects (mean age: 16.2±3 years, mean BMI-SDS: 2.17±0.05) were enrolled the study. The diagnosis of PCOS was established according to the Rotterdam criteria. Hyperinsulinism and insulin resistance was evaluated using the homeostasis model assessment (HOMA-IR) from fasting samples. Plasma adiponectin and vaspin levels were determined by radioimmunoassay. Determination of visfatin and apelin levels was performed by enzyme immunoassay. RESULTS: HOMA-IR, apelin and visfatin levels (4.9±2 versus 1.4±0.7, p<0.001; 2.2±1.1 versus 0.58±0.16, p<0.001; 31.3±11.1 versus 18.5±10.7, p<0.001; respectively) were significantly elevated, and adiponectin levels (2.01±1.02 versus 12.5±6.2, p<0.001) were significantly lower in the PCOS group. Vaspin levels were higher in the PCOS group than in the control group, but the differences were not significant. Apelin and visfatin correlated positively and adiponectin correlated negatively with BMI-SDS and HOMA-IR. CONCLUSION: Based on the findings of this study, apelin, visfatin and adiponectin levels can be used as specific markers for insulin sensitivity, and these adipocytokines might play a part in the pathogenesis of PCOS.
AIM: The aim of this study was to investigate the relationship between four circulating adipocytokines (apelin, vaspin, visfatin, adiponectin) and markers of insulin sensitivity, in the context of polycystic ovary syndrome (PCOS) in adolescents. SUBJECTS AND METHODS: 48, obese, adolescent girls (mean age: 15.6±3.4 years, mean body mass index standard deviation score (BMI-SDS): 2.31±0.1), and 37 control subjects (mean age: 16.2±3 years, mean BMI-SDS: 2.17±0.05) were enrolled the study. The diagnosis of PCOS was established according to the Rotterdam criteria. Hyperinsulinism and insulin resistance was evaluated using the homeostasis model assessment (HOMA-IR) from fasting samples. Plasma adiponectin and vaspin levels were determined by radioimmunoassay. Determination of visfatin and apelin levels was performed by enzyme immunoassay. RESULTS: HOMA-IR, apelin and visfatin levels (4.9±2 versus 1.4±0.7, p<0.001; 2.2±1.1 versus 0.58±0.16, p<0.001; 31.3±11.1 versus 18.5±10.7, p<0.001; respectively) were significantly elevated, and adiponectin levels (2.01±1.02 versus 12.5±6.2, p<0.001) were significantly lower in the PCOS group. Vaspin levels were higher in the PCOS group than in the control group, but the differences were not significant. Apelin and visfatin correlated positively and adiponectin correlated negatively with BMI-SDS and HOMA-IR. CONCLUSION: Based on the findings of this study, apelin, visfatin and adiponectin levels can be used as specific markers for insulin sensitivity, and these adipocytokines might play a part in the pathogenesis of PCOS.