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 < HOMA(IR), 0.005) and a lower fasting glucose-to-insulin ratio (G(0)/I(0)) (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 HOMA(IR). After adjusting insulin resistance index of HOMA(IR) 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.
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 < HOMA(IR), 0.005) and a lower fasting glucose-to-insulin ratio (G(0)/I(0)) (P < 0.001) than controls. CD36 protein levels in the PCOSwomen 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 HOMA(IR). After adjusting insulin resistance index of HOMA(IR) 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.
Authors: Oleg Varlamov; Michael P Chu; Whitney K McGee; Judy L Cameron; Robert W O'Rourke; Kevin A Meyer; Cecily V Bishop; Richard L Stouffer; Charles T Roberts Journal: Endocrinology Date: 2013-09-05 Impact factor: 4.736