Jing Zhang1, Lingling Zhou, Liulin Tang, Liangzhi Xu. 1. Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, 610041, People's Republic of China.
Abstract
OBJECTIVES: To investigate the relationship between plasma resistin, polycystic ovary syndrome (PCOS), and insulin resistance (IR). To compare the mRNA level of resistin in mononuclear cells and monocyte-derived macrophages in women with PCOS and controls. MATERIALS AND METHODS: Patients with PCOS and controls were enrolled and IR was considered as the stratified factor for subgroups. Fasting blood was collected to determine the levels of sex hormones, insulin, glucose, blood lipid, and resistin. Resistin gene expression was evaluated by quantitative real-time RT-PCR in mononuclear cells and monocyte-derived macrophages cultured with or without rosiglitazone for 96 h. RESULTS: No significant difference of plasma resistin levels was found among PCOS-IR, PCOS-non-IR, control-IR, and control-non-IR groups. There were no significant differences in resistin mRNA expression between participants with and without PCOS and with and without IR. Resistin mRNA expression in monocyte-derived macrophages was higher than that in mononuclear cells (p = 0.04), and could be reduced by rosiglitazone (p < 0.001). CONCLUSIONS: Plasma resistin does not correlate with normal weight PCOS or IR. Resistin gene expression in mononuclear cells and monocyte-derived macrophages in PCOS and IR is the same as controls. Further researches on the role of resistin in the pathogenesis of PCOS or IR should concentrate on the tissue level.
OBJECTIVES: To investigate the relationship between plasma resistin, polycystic ovary syndrome (PCOS), and insulin resistance (IR). To compare the mRNA level of resistin in mononuclear cells and monocyte-derived macrophages in women with PCOS and controls. MATERIALS AND METHODS:Patients with PCOS and controls were enrolled and IR was considered as the stratified factor for subgroups. Fasting blood was collected to determine the levels of sex hormones, insulin, glucose, blood lipid, and resistin. Resistin gene expression was evaluated by quantitative real-time RT-PCR in mononuclear cells and monocyte-derived macrophages cultured with or without rosiglitazone for 96 h. RESULTS: No significant difference of plasma resistin levels was found among PCOS-IR, PCOS-non-IR, control-IR, and control-non-IR groups. There were no significant differences in resistin mRNA expression between participants with and without PCOS and with and without IR. Resistin mRNA expression in monocyte-derived macrophages was higher than that in mononuclear cells (p = 0.04), and could be reduced by rosiglitazone (p < 0.001). CONCLUSIONS: Plasma resistin does not correlate with normal weight PCOS or IR. Resistin gene expression in mononuclear cells and monocyte-derived macrophages in PCOS and IR is the same as controls. Further researches on the role of resistin in the pathogenesis of PCOS or IR should concentrate on the tissue level.