Visceral adiposity and insulin resistance in polycystic ovarian syndrome - A cross-sectional, observational study

Insulin resistance (IR) is the pathogenic mechanism responsible for polycystic ovarian syndrome (PCOS) and excess of visceral adipose tissue (VAT).

We examined VAT and IR using the homeostasis model assessment (HOMA) in patients with PCOS and controls.

In this cross-sectional, observational study, we included 74 patients newly diagnosed with PCOS and a similar number of age- and weight-matched healthy women as controls. Haematological, biochemical, and hormonal parameters were estimated from a fasting blood sample taken during the follicular phase, and VAT was assessed using dual-energy X-ray absorptiometry (DEXA). The results were analyzed using relevant statistical methods, and a p-value of less than 0.05 was considered significant.

The study participants (n = 148) had a mean age of 23.6 ± 3.7 years, body weight of 59.9 ± 11.6 kg, and a body mass index (BMI) of 25.2 ± 3.2 kg/m². Among the PCOS patients, 25 had a normal BMI and 49 were obese. The VAT (grams) was comparable between patients (484.3 ± 218.2) and controls (439.9 ± 212.8) (p = 0.1591). The percentage of fat in the trunk/legs was higher in PCOS patients (0.9 ± 0.1) than controls (0.87 ± 0.08) (p = 0.0329). Correlation analysis revealed a positive correlation of 17-hydroxy progesterone (17OHP) with many adiposity parameters in both groups (p < 0.001).

The VAT was similar in PCOS and controls, and HOMA showed significant correlation with VAT. 17 OHP correlated with many metabolic and hormonal parameters in both groups. Further studies with larger sample sizes are needed to confirm our findings.