Background: Polycystic ovary syndrome (PCOS) is associated with features linked to metabolic syndrome including visceral obesity, dyslipidemia and impaired glucose homeostasis. Recent studies suggest that these metabolic effects are linked to a low-grade chronic inflammation with the triad of hyperinsulinemia, hyperandrogenism, and low-grade inflammation acting together in a vicious cycle. Adipose tissue produces immunomodulatory adipocytokines which contribute to regulation of insulin sensitivity, reproduction and cardiovascular function. Limited evidence is available on the role of adipocytokines in PCOS.
Aims: This study investigated the relationships between PCOS status, adipocytokines and aetiological features of PCOS.
Methods: In an observational study of community recruited PCOS and controls, we measured serum HMW-adiponectin, omentin, resistin, interleukin-6 (IL-6), asymmetric dimethylarginine (ADMA), plasminogen activator inhibotir-1(PAI-1), high sensitivity CRP (hs-CRP), androgens, SHBG, fasting glucose and insulin levels.
Results: 49 women with PCOS (age 29.8±5.9 years, BMI: 29.0±5.4 kg/m2) and 25 healthy controls (age 37.6±7.8 years, BMI: 28.9±4.0 kg/m2) were recruited. Homeostatic model assessment for insulin resistance (HOMA-IR) (P=0.006), free androgen index (FAI) (P=0.01) and Ferriman-Galway score (P<0.001) were higher in PCOS. For adipocytokines, women with PCOS had lower omentin [median (IQR): 68.76(67.17) vs 112.45(67.42)] (P=0.01) and higher hs-CRP [median (IQR): 2.15 (3.4) vs 1.00 (2.1)] (P=0.03) after adjustment for age and BMI. On assessment of non-obese and obese subgroups, HMW-adiponectin and omentin were lower in obese women with PCOS compared to obese controls (P=0.022 and P=0.034 respectively) and non-obese PCOS (P=0.028 and P=0.016 respectively). Among women with PCOS, HMW-adiponectin was negatively correlated with HOMA-IR and FAI, however only the correlation between HMW-adiponectin and FAI remained significant (P=0.03) after adjustment for BMI.
Conclusion: Overall, adipocytokines and inflammation appear abnormal in PCOS. In the obese subgroup abnormalities were more marked in PCOS than in controls. This is consistent with the presence of an inflammatory state and dysfunctional adipose tissue in PCOS.