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作 者:初永丽[1] 邱红玉[2] 孙永玉[2] 李旻[2] 李红发[2]
机构地区:[1]山东省烟台毓璜顶医院妇产科,烟台264000 [2]华中科技大学同济医学院附属协和医院妇产科
出 处:《现代妇产科进展》2007年第11期839-842,共4页Progress in Obstetrics and Gynecology
基 金:烟台市科技发展计划基金资助项目(No:2004221)
摘 要:目的:研究多囊卵巢综合征(polycystic ovary syndrome,PCOS)患者脂肪组织胰岛素受体底物-1(insulin receptor substrate-1,IRS-1)及胰岛素受体底物-2(insulin recep-tor substrate-2,IRS-2)蛋白的表达及其酪氨酸磷酸化,探讨PCOS产生胰岛素抵抗(insulinresistance,IR)的分子机制。方法:用放射免疫法检测各实验组血清促黄体生成素(luteini-zing hormone,LH)、促卵泡激素(follicle stimulating hormone,FSH)、睾酮(testosterone,T)、血清空腹胰岛素(fasting insulin,FIN)的水平;用葡萄糖氧化酶法测定血浆空腹血糖(fast-ing plasma glucose,FPG);用HOMA(homeostasis model assessment,HOMA)模型计算胰岛素抵抗指数(HOMA-IR);用Western blot检测IRS-1及IRS-2蛋白的表达,应用免疫沉淀及增强化学发光法检测二者的酪氨酸磷酸化程度。结果:(1)PCOS IR组患者血清LH、LH/FSH、T、FIN及HOMA-IR均显著高于PCOS非IR组与对照组(均P(0.05);(2)PCOSIR组与PCOS非IR组及对照组相比,IRS-1蛋白表达量明显下降(P(0.05),IRS-2蛋白表达差异无统计学意义(P>0.05);(3)PCOS IR组IRS-1及IRS-2蛋白质酪氨酸磷酸化程度显著降低(均P(0.05)。结论:PCOS患者脂肪组织IRS-1蛋白表达下降,IRS-1及IRS-2蛋白质酪氨酸磷酸化程度降低,由此导致的受体后信号转导障碍可能是产生胰岛素抵抗的机制之一。Objective:To investigate the tyrosine phosphorylation and protein expressions of insulin receptor substrate-1 and 2 in adipose tissue from patients with polycystic ovary syndrome,and explore molecular mechanisms of insulin resistance of PCOS. Methods:Serum luteinizing hormone ( LH ), follicle stimulating hormone ( FSH ), testosterone (T) and fasting insulin (FIN) were measured by chemiluminescence assay. Fasting plasma glucose (FPG) was measured by oxidase assay. The abundance of insulin receptor substrate-1 and 2 in adipose tissue was assessed by Western blot. The tyrosine phosphorylation of IRS-1 and IRS-2 was measured by immunoprecipitation and enhanced chemiluminescent immunoblotting technique. Resuits: (1) The levels of serum LH,LH/FSH,T,FIN and HOMA-IR in PCOS without insulin resistance were significantly higher than those of control group ( all P 〈 0.05 ) ; (2) The protein expression of IRS-1 in PCOS with insulin resistance was significantly lower than those in PCOS without insulin resistance and control group( P 〈 0.05 ) ;(3 )The tyrosine phosphorylation analysis of IRS-1 and IRS-2 were both significantly decreased in PCOS with insulin resistance compared to that of PCOS without insulin resistance and control groups (P 〈 0.05 ). Conclusion: Because of decreased IRS-1 and IRS-2 in the insulin insulin resistance.
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