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

Kok Min Seow, Yieh Loong Tsai, Jiann Loung Hwang, Wei Yen Hsu, Low Tone Ho, Chi Chang Juan

Research output: Contribution to journalArticle

14 Citations (Scopus)

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 languageEnglish
Pages (from-to)1982-1988
Number of pages7
JournalHuman Reproduction
Volume24
Issue number8
DOIs
Publication statusPublished - Aug 2009

Fingerprint

CD36 Antigens
Sterol Esterase
Polycystic Ovary Syndrome
Adipose Tissue
Insulin
Lipase
Insulin Resistance
Fasting
Nonesterified Fatty Acids
Proteins
Lipolysis
Serum
Testosterone
Homeostasis
Western Blotting
Glucose

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 journalArticle

Seow, Kok Min ; Tsai, Yieh Loong ; Hwang, Jiann Loung ; Hsu, Wei Yen ; Ho, Low Tone ; Juan, Chi Chang. / Omental adipose tissue overexpression of fatty acid transporter CD36 and decreased expression of hormone-sensitive lipase in insulin-resistant women with polycystic ovary syndrome. In: Human Reproduction. 2009 ; Vol. 24, No. 8. pp. 1982-1988.
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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.",
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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

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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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