Hum. Reprod. Advance Access published online on May 7, 2009
Human Reproduction, doi:10.1093/humrep/dep122
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Omental adipose tissue overexpression of fatty acid transporter CD36 and decreased expression of hormone-sensitive lipase in insulin-resistant women with polycystic ovary syndrome
1 Department of Obstetrics and Gynecology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan 2 School of Medicine, Fu-Jen Catholic University, Taipei Hsien, Taiwan 3 Department of Obstetrics and Gynecology, Taipei Medical University, Taipei, Taiwan 4 Institute of Physiology, National Yang-Ming University, Taipei 112 Taiwan 5 Department of Medical Research & Education, Taipei Veterans General Hospital, Taipei, Taiwan 6 Department of Internal Medicine, Taipei Veterans General Hospital, Taipei, Taiwan 7 Department of Education and Research, Taipei City Hospital, Taipei, Taiwan
8 Correspondence address. Tel: +886-2-2826-7000; Fax: +886-2-2826-4051; E-mail: ccjuan{at}ym.edu.tw
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.
Key words: polycystic ovary syndrome/free fatty acids/CD36/hormone-sensitive lipase
Submitted on December 25, 2008; resubmitted on March 26, 2009; accepted on April 9, 2009.