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

Oleh:

Kok-Min, Seow ; Yieh-Loong, Tsai ; Jiann-Loung, Hwang ; Wei-Yen, Hsu

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Human Reproduction vol. 24 no. 08 (Aug. 2009), page 1982-1988.
Topik: polycystic ovary syndrome/free fatty acids/CD36/hormone-sensitive lipase

Ketersediaan

Perpustakaan FK Nomor Panggil: H07.K Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

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.

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