TY - JOUR
T1 - Omental adipose tissue overexpression of fatty acid transporter CD36 and decreased expression of hormone-sensitive lipase in insulin-resistant women with polycystic ovary syndrome
AU - Seow, Kok Min
AU - Tsai, Yieh Loong
AU - Hwang, Jiann Loung
AU - Hsu, Wei Yen
AU - Ho, Low Tone
AU - Juan, Chi Chang
N1 - Funding Information:
Acknowledgment. We would like to express our sincere thanks for the reviewer for his valuable comments on this paper that made this paper complete and significant. Also, the authors would like to thank Prince Sultan University for funding this work through research group Nonlinear Analysis Methods in Applied Mathematics (NAMAM) group number RG-DES-2017-01-17.
PY - 2009/8
Y1 - 2009/8
N2 - 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.
AB - 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.
KW - CD36
KW - Free fatty acids
KW - Hormone-sensitive lipase
KW - Polycystic ovary syndrome
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U2 - 10.1093/humrep/dep122
DO - 10.1093/humrep/dep122
M3 - Article
C2 - 19423542
AN - SCOPUS:67651123047
SN - 0268-1161
VL - 24
SP - 1982
EP - 1988
JO - Human Reproduction
JF - Human Reproduction
IS - 8
ER -