Omental adipose tissue overexpression of fatty acid transporter CD36 and decreased expression of hormone-sensitive lipase in insulin-resistant women with polycystic ovary syndrome

BACKGROUND Elevated free fatty acids (FFAs) are involved in insulin resistance in polycystic ovary syndrome (PCOS). We investigated the role of fatty acid transporter CD36, hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) in regulation of lipolysis in insulin-resistant women with PCOS. METHODS CD36, HSL and ATGL proteins were analyzed in omental adipose tissue from 10 women with PCOS and 10 healthy, BMI- and age-matched controls by western blotting. RESULTS Women with PCOS had higher fasting and 2 h insulin levels (P < 0.002, P < 0.029, respectively) and a higher homeostasis model insulin resistance index (P < HOMAIR, 0.005) and a lower fasting glucose-to-insulin ratio (G0/I0) (P < 0.001) than controls. CD36 protein levels in the PCOS women were higher (268% of control levels, P < 0.05) and HSL protein levels were lower (43% of control levels, P < 0.05). However, ATGL protein levels were not different in the two groups. Fasting serum insulin levels showed a positive correlation with CD36 levels (P = 0.01, r = 0.875) and a negative correlation with HSL levels (P = 0.045, r = −0.73). Furthermore, a positive correlation was found between serum testosterone levels and CD 36 protein levels (P = 0.025, r = 0.817) but the correlation did not reach significance after controlling for HOMAIR. After adjusting insulin resistance index of HOMAIR by analysis of covariance, only CD36 differed between PCOS and control (P = 0.026). CONCLUSIONS Our results suggest that, in insulin-resistant women with PCOS, changes in CD36 and HSL expression may result in altered FFA uptake.