Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 1982-1988 |
| Number of pages | 7 |
| Journal | Human Reproduction |
| Volume | 24 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - Aug 2009 |
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Keywords
- CD36
- Free fatty acids
- Hormone-sensitive lipase
- Polycystic ovary syndrome
ASJC Scopus subject areas
- Rehabilitation
- Obstetrics and Gynaecology
- Reproductive Medicine
Cite this
Omental adipose tissue overexpression of fatty acid transporter CD36 and decreased expression of hormone-sensitive lipase in insulin-resistant women with polycystic ovary syndrome. / Seow, Kok Min; Tsai, Yieh Loong; Hwang, Jiann Loung; Hsu, Wei Yen; Ho, Low Tone; Juan, Chi Chang.
In: Human Reproduction, Vol. 24, No. 8, 08.2009, p. 1982-1988.Research output: Contribution to journal › Article
}
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
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
UR - http://www.scopus.com/inward/record.url?scp=67651123047&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=67651123047&partnerID=8YFLogxK
U2 - 10.1093/humrep/dep122
DO - 10.1093/humrep/dep122
M3 - Article
C2 - 19423542
AN - SCOPUS:67651123047
VL - 24
SP - 1982
EP - 1988
JO - Human Reproduction
JF - Human Reproduction
SN - 0268-1161
IS - 8
ER -