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目的检测多囊卵巢综合征(PCOS)患者脂肪组织胰岛素受体底物(IRS)2蛋白表达及其酪氨酸磷酸化的程度,探讨发生PCOS合并胰岛素抵抗(IR)的机制。方法采用蛋白印迹(Westernblot)法,检测PCOS合并IR患者19例(PCOS合并IR组)、PCOS非IR患者17例(PCOS非IR组)及因单纯子宫肌瘤行子宫切除术的患者20例(对照组)的IRS2蛋白的表达;并采用免疫组化技术,检测IRS2在脂肪组织中的分布;采用免疫沉淀及增强化学发光法,检测IRS2的酪氨酸磷酸化程度。结果(1)PCOS合并IR组、PCOS非IR组及对照组IRS2蛋白表达分别为115±026、113±026及100±025,3组比较,差异无统计学意义(P>005)。(2)PCOS合并IR组、PCOS非IR组及对照组IRS2蛋白酪氨酸磷酸化程度分别为077±016、091±025及100±012,3组比较,差异有统计学意义(P<005);PCOS非IR组与对照组比较,差异无统计学意义(P>005)。结论PCOS合并IR患者脂肪组织的IRS2蛋白酪氨酸磷酸化程度的降低,可能是发生IR的机制之一。
Objective To investigate the expression of insulin receptor substrate (IRS) 2 and its tyrosine phosphorylation in patients with polycystic ovary syndrome (PCOS) and to explore the mechanism of PCOS combined with insulin resistance (IR). Methods Western blotting was used to detect 19 patients with PCOS complicated with IR (PCOS combined IR group), 17 patients with PCOS non-IR (PCOS non-IR group) and 20 patients with hysteromyoma Control group). The expression of IRS2 in adipose tissue was detected by immunohistochemistry. The tyrosine phosphorylation of IRS2 was detected by immunoprecipitation and enhanced chemiluminescence. Results (1) The expression of IRS2 protein in PCOS combined IR group, PCOS non-IR group and control group were 115 ± 026,113 ± 026 and 100 ± 025 respectively, there was no significant difference between the 3 groups (P> 0.05). (2) The levels of tyrosine phosphorylation of IRS2 protein in PCOS combined IR group, PCOS non-IR group and control group were 077 ± 016,091 ± 025 and 100 ± 012 respectively, there was significant difference (P <0.05 ); PCOS non-IR group compared with the control group, the difference was not statistically significant (P> 005). Conclusion The decrease of IRS2 tyrosine phosphorylation in adipose tissue of patients with PCOS complicated with IR may be one of the mechanisms of IR.