BACKGROUNDElevated 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.METHODSCD36, 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.RESULTSWomen 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).CONCLUSIONSOur results suggest that, in insulin-resistant women with PCOS, changes in CD36 and HSL expression may result in altered FFA uptake.
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