Wang Zhu-chen, Gu Xiong-fei, Yang Dong-zi, Kuang Jian-quan
Department of Obstetrics and Gynecology, Second Affiliated Hospital, Sun Yat-sen University, Guangzhou 510120, China.
Zhonghua Fu Chan Ke Za Zhi. 2005 Feb;40(2):120-3.
To study expression of insulin receptor substrate 1 (IRS-1) and phosphorylation of tyrosine in adipose tissue of polycystic ovary syndrome (PCOS) to approach the mechanism of insulin resistance (IR) in PCOS at tissue and cellular level.
IRS-1 expression and tyrosine phosphorylation of adipose tissue were studied with immunoprecipitation, Western-blot and ECL immunoblotting.
The differences of IRS-1 expression in adipose tissue among the obese PCOS group (82 +/- 15)%, the non-obese PCOS group (79 +/- 18)%, the obese control group (75 +/- 19)% and the non obese control group (70 +/- 19)% were not significant (P > 0.05). IRS-1 tyrosine phosphorylation in adipose tissue in the obese PCOS group [(52 +/- 23)%, P < 0.001], the obese control group [(45 +/- 22)%, P < 0.01] and non-obese PCOS group [(70 +/- 25)%, P < 0.05] were markedly lower than that in the non-obese control group (88 +/- 12)%. The obese control group had more reduction than non-obese control group (P < 0.05). The differences between the obese PCOS group and the obese control group or the two PCOS groups were not significant (P > 0.05).
IRS-1 tyrosine phosphorylation in adipose tissue in the two PCOS groups decreased markedly than in the non-obese control group. It might be involved in the disorder of insulin-signaling transduction downstream of insulin receptor and the occurrence of IR.
研究多囊卵巢综合征（PCOS）患者脂肪组织中胰岛素受体底物1（IRS-1）的表达及酪氨酸磷酸化情况，从组织和细胞水平探讨PCOS胰岛素抵抗（IR）的机制。
采用免疫沉淀、蛋白质免疫印迹（Western-blot）及增强型化学发光免疫印迹（ECL免疫印迹）法研究脂肪组织中IRS-1表达及酪氨酸磷酸化情况。
肥胖PCOS组（82±15）%、非肥胖PCOS组（79±18）%、肥胖对照组（75±19）%和非肥胖对照组（70±19）%脂肪组织中IRS-1表达差异无统计学意义（P>0.05）。肥胖PCOS组[（52±23）%，P<0.001]、肥胖对照组[（45±22）%，P<0.01]及非肥胖PCOS组[（70±25）%，P<0.05]脂肪组织中IRS-1酪氨酸磷酸化水平均显著低于非肥胖对照组（88±12）%。肥胖对照组降低幅度大于非肥胖对照组（P<0.05）。肥胖PCOS组与肥胖对照组或两组PCOS组间差异无统计学意义（P>0.05）。
两组PCOS患者脂肪组织中IRS-1酪氨酸磷酸化水平均显著低于非肥胖对照组，可能参与胰岛素受体下游胰岛素信号转导紊乱及IR的发生。
