Full Title: Increased regulated on activation, normal T-cell expressed and secreted levels and cysteine–cysteine chemokine receptor 5 upregulation in omental adipose tissue and peripheral blood mononuclear cells are associated with testosterone level and insulin resistance in polycystic ovary syndrome
Chi-Chang Juan, Ph.D., Kuo-Hu Chen, M.D., Chien-Wei Chen, Ph.D., Chi-Hong Ho, M.D., Ph.D., Peng-Hui Wang, M.D., Ph.D., Harn-Shen Chen, M.D., Ph.D., Jiann-Loung Hwang, M.D., Yu-Hung Lin, M.D., Kok-Min Seow, M.D., Ph.D.
To study the relationship between circulating chemokine cysteine–cysteine motif ligand (CCL) 5 levels and cysteine–cysteine chemokine receptor type 5 (CCR5) expression in peripheral blood mononuclear cells (PBMCs) and adipose tissue with hyperandrogenism and insulin resistance in patients with polycystic ovary syndrome (PCOS).
University teaching hospital.
Fifteen women with PCOS and 15 controls matched for body mass index and age were enrolled in this study.
Main Outcome Measure(s)
Plasma levels of CCL3, CCL4, and CCL5 were determined using enzyme-linked immunosorbent assay kits, and omental adipose tissue and PBMCs were analyzed using real-time polymerase chain reaction to determine the expression level of CCR5 in participants.
Levels of CCL5 were significantly higher in women with PCOS. Expression of CCR5 in adipose tissue and PBMCs was significantly higher in women with PCOS compared with that in women in the control group. Cysteine–cysteine chemokine receptor type 5 expression also was upregulated in THP-1 cells after chronic exposure to testosterone. Levels of CCL5 had a significant positive correlation with testosterone levels in women with PCOS. Moreover, CCR5 showed a positive correlation with fasting glucose levels, homeostasis model insulin resistance index, and C-reactive protein.
Increased levels of CCL5 and overexpression of CCR5 in PBMCs and adipose tissue are associated with hyperandrogenism and insulin resistance in women with PCOS. Additionally, CCR5 and CCL5 may be used as biomarkers in the pathogenesis of PCOS.