IGF-I与子宫内膜异位症相关关系的研究

目的 观察胰岛素样生长因子-I(IGF-I)及其受体(IGF-IR)在子宫腺肌症患者原位及异位内膜表达,以探讨子宫腺肌症发生维持及侵袭的机制.方法 取20例子宫腺肌症患者的原位和异位内膜标本作为病例组,另取22例正常内膜作为对照组.采用免疫组织化学方法检测IGF-I,IGF-IR的分布及表达.结果 正常内膜及子宫腺肌症的原位和异位内膜组织中均有IGF-I,IGF-IR的表达,IGF-I在异位内膜组织中表达较高(P＜0.05＝.结论 IGF-I可能参与子宫腺肌症的异位内膜生长与维持.     

GLUT4在多囊卵巢综合征大鼠子宫内膜中的表达及意义

目的： 探讨葡萄糖转移因子4（GLUT4）在多囊卵巢综合征（PCOS）大鼠子宫内膜中的表达，评价其与子宫内膜胰岛素抵抗(IR)的关系。方法: 54只85日龄SD雌性大鼠，随机分为：① 对照组（20只）；② PCOS组（17只）；③ 二甲双胍治疗组（17只）。其中后两组先参照Poretsky等的方法复制PCOS大鼠模型，造模成功后，再分别喂服安慰剂或二甲双胍， 14 d后断头处死各组大鼠并取材。采用免疫组织化学染色Elivision^TM Plus两步法检测对照组、PCOS组及治疗组大鼠子宫内膜GLUT4蛋白的表达。结果: PCOS组大鼠子宫内膜腺上皮中GLUT4和INS-R蛋白表达明显低于对照组（P＜0.01，P＜0.05），INS蛋白表达水平明显高于对照组水平（P＜0.01）；治疗组GLUT4表达显著高于PCOS组（P＜0.01），但仍低于对照组（P＜0.01），INS表达较PCOS组显著降低（P＜0.05），但仍高于对照组（P＜0.05）；子宫内膜间质中无GLUT4的表达，INS和INS-R表达情况与腺上皮相似。结论: PCOS大鼠子宫内膜GLUT4表达减少和子宫内膜的IR有关。     

卵巢局部IGF-I系统与多囊卵巢综合征胰岛素抵抗的相关性研究

目的：研究卵巢局部胰岛素样生长因子-I系统（IGF-I系统）在伴有胰岛素抵抗多囊卵巢综合征中的作用机制。方法选择30例合并胰岛素抵抗的PCOS（polycystic ovary syndrome）患者为试验组,30例患有卵巢良性肿瘤需手术探查的患者为对照组。检测并对比血清、小卵泡液中IGF-I、胰岛素样生长因子结合球蛋白-1（IGFBP-1）与各项性激素,FI,2hI,ISI,QUICK I,卵巢超声指标,研究其与各种指标间的相关性。结果试验组小卵泡液IGF-I高于对照组（P〈0.01）,小卵泡液及血清IGFBP-1低于对照组（P〈0.05,P〈0.01）。试验组小卵泡液IGF-I水平高于血清（P〈0.01）,小卵泡液IGFBP-1水平低于血清（P〈0.05）。试验组小卵泡液IGF-I与T0、E2及卵巢体积（OV）,卵巢总面积（TA）,卵泡数（FN）,空腹胰岛素（FI）,服糖后2h胰岛素（2hI）呈正相关（P〈0.05）;血清IGF-I与胰岛素敏感指数（ISI）,体重指数（BMI）,腰臀比（WHR）呈正相关（P〈0.05）,与定量胰岛素敏感指数（QUICK I）呈负相关（P〈0.05）;试验组小卵泡液及血清IGFBP-1与FI,2hI呈负相关（P〈0.05）。结论 IR可能通过影响卵巢局部IGF-I系统,刺激卵巢分泌雄激素,引发排卵障碍,在PCOS的发病机制中起到重要作用。     

多囊卵巢综合征患者血清IGF-1水平与胰岛素抵抗

目的探讨血清胰岛素样生长因子1(IGF-1)、胰岛素敏感指数(ISI)与多囊卵巢综合征(PCOS)的关系。方法采集90例PCOS患者和41例正常对照组血清,应用电化学发光法检测胰岛素水平,葡萄糖氧化酶终点法检测空腹葡萄糖(FPG)水平,酶联免疫吸附试验(ELISA)检测IGF-1水平。结果 1.PCOS患者FPG、血清胰岛素、IGF-1水平明显高于正常对照组(t=16.72,2.24,4.51;P<0.01),且均与患者是否肥胖高度相关(t=5.08,2.07,3.30;P<0.01);2.PCOS患者胰岛素敏感性明显低于对照组,差别有显著性意义(t=3.12,P<0.05);3.PCOS患者血清IGF-1的含量与胰岛素敏感指数呈显著负相关,差别有显著性意义(r=-0.57,P<0.05);对照组血清IGF-1含量与胰岛素敏感指数无明显相关性(r=0.14,P>0.05)。结论多囊卵巢综合征患者存在不同程度的胰岛素抵抗(IR),IGF-1水平增高与PCOS患者发生IR有关,IGF-1可能与PCOS发生、发展有一定的内在联系并起协同作用。     

多囊卵巢综合征大鼠骨骼肌细胞胰岛素受体底物1及其丝氨酸307位点磷酸化的表达

背景：胰岛素受体底物1的丝氨酸307位点磷酸化程度的增加参与了骨骼肌胰岛素抵抗的发生。 目的：观察多囊卵巢综合征大鼠骨骼肌细胞胰岛素受体底物1的含量及其丝氨酸307位点磷酸化程度的变化。 方法：将大鼠随机分为模型组和对照组,模型组给予人绒毛膜促性腺激素联合胰岛素皮下注射,并配以高脂饮食,构建大鼠多囊卵巢综合征模型;对照组皮下注射生理盐水,正常饲料喂养。 结果与结论：干预6周后,Western blot检测结果显示,与对照组相比,模型组大鼠骨骼肌细胞胰岛素受体底物1表达量显著下降(P < 0.05),而其丝氨酸307位点磷酸化蛋白表达明显升高(P < 0.05)。结果提示,多囊卵巢综合征大鼠骨骼肌细胞中胰岛素受体底物1蛋白表达下调及其丝氨酸307位点磷酸化蛋白表达上调与多囊卵巢综合征大鼠骨骼肌胰岛素抵抗的发生密切相关。     

多囊卵巢综合征胰岛素抵抗患者Gly972Arg多态性与子宫内膜胰岛素受体底物1表达的关系

目的:研究多囊卵巢综合征(Polycystic ovary syndrome,PCOS)胰岛素抵抗(Insulin resistance,IR)患者胰岛素受体底物1(Insulin receptor substrate,IRS-1)基因Gly972Arg多态性与子宫内膜IRS-1表达的关系。方法:PCOS患者51例,用聚合酶链反应(PCR)技术,检测IRS-1Gly972Arg多态性。于月经周期第1天刮取子宫内膜,合并胰岛素抵抗者28例,非胰岛素抵抗者23例,应用免疫组化技术检测子宫内膜IRS-1,计算机图像分析系统分析子宫内膜IRS-1的表达。结果:Gly972Arg多态性:51例PCOS患者中,基因型GG 49例,基因型GA 2例,IR组与无IR组各1例,两组比较无统计学意义。子宫内膜IRS-1的表达:IR组、非IR组IRS-1表达的灰度值分别为131.94±18.39、78.16±6.87,比较有统计学意义(P<0.01)。结论:IRS-1Gly972Arg的突变率较低,其多态性在PCOS IR组与无IR组比较无统计学意义(P>0.05),不影响子宫内膜IRS-1的表达。     

IGF-Ⅰ与子宫内膜异位症相关关系的研究

目的观察胰岛素样生长因子-Ⅰ（IGF-Ⅰ）及其受体（IGF-IR）在子宫腺肌症患者原位及异位内膜表达。以探讨子宫腺肌症发生维持及侵袭的机制。方法取20例子宫腺肌症患者的原位和异位内膜标本作为病例组，另取22例正常内膜作为对照组。采用免疫组织化学方法检测IGF-Ⅰ，IGF-IR的分布及表达。结果正常内膜及子宫腺肌症的原位和异位内膜组织中均有IGF-Ⅰ，IGF-IR的表达，IGF-Ⅰ在异位内膜组织中表达较高（P〈0．05）。结论IGF-Ⅰ可能参与子宫腺肌症的异位内膜生长与维持。     

子宫内膜异位症患者血清中胰岛素样生长因子Ⅰ(IGF1)水平变化的意义

目的探索子宫内膜异位症患者血清IGF1水平变化与子宫内膜异位症发病的关系。方法采用双抗体夹心ABC ELISA法测定36例子宫内膜异位症患者及24例健康妇女IGF1水平。结果(1)子宫内膜异位症组血清IGF1水平为(284.4±86.6)ng/m l,对照组血清IGF1水平为(138.2±74.1)ng/m l。子宫内膜异位症组血清IGF1水平高于对照组血清IGF1水平,两组比较,差异有显着性(P<0.05)。(2)两组妇女分别进行增生期与分泌期血清中IGF1水平比较,正常组妇女增生期与分泌期血清中IGF1水平比较,差异无显著性(P>0.05)。子宫内膜异位症组妇女增生期与分泌期血清中IGF1水平比较,差异无显着性(P>0.05)。结论血清中IGF1水平变化与子宫内膜异位症的发病密切相关。     

子痫前期患者血清及胎盘中IGF-I、瘦素水平变化及相关性研究

目的:探讨子痫前期患者血清及胎盘中胰岛素样生长因子-I(IGF-I)、瘦素(leptin)水平变化及其相互关系。方法:采用酶联免疫吸附法及免疫组织化学法分别检测80例重度子痫前期患者和50例正常妊娠妇女血清及胎盘组织中IGF-1、leptin的水平。结果:轻度和重度子痫前期组孕妇分娩前和脐静脉血IGF-I水平均明显低于对照组孕妇,leptin水平均明显高于对照组孕妇,且随子痫前期的病情加重,分娩前和脐静脉血IGF-I水平亦随之降低,leptin水平亦随之增加,各组两两比较有显著性差异(P<0.05)。在对照组、轻度子痫前期组、重度子痫前期组胎盘组织中IGF-I和leptin的表达比较有显著性差异(P<0.05)。结论:IGF-I和leptin可能参与了子痫前期的发生发展过程,且可作为监测患者病情变化的参考指标。     

IGF-I和IGF-IR在高氧致新生鼠慢性肺疾病中的动态表达及其作用

目的研究IGF-I、IGF-IR在高氧致新生鼠慢性肺疾病（CLD）中的表达及作用。方法将足月新生大鼠144只随机分为高氧组和空气组,分别于实验1d,3d,7d,10d,14d,21d应用免疫组化和RT-PCR技术检测IGF-I、IGF-IR的动态表达。结果CLD时IGF-I和IGF-IR呈动态变化,高氧组和空气组比较,在实验3d～10d IGF-I和IGF-IR表达明显降低（P〈0.05）,14d和21d表达明显增强（P〈0.05）。结论IGF-I和IGF-IR是肺泡发育的正向调节因子,与CLD时肺泡分隔受阻、肺泡成熟障碍和肺纤维化有关。     

Birth insults involving hypoxia produce long-term increases in hippocampal [125I]insulin-like growth factor-I and -II receptor binding in the rat

Insulin-like growth factors-I and -II and insulin are structurally related mitogenic growth factors with multiple actions in the developing nervous system and adult CNS. Previous studies have demonstrated acute induction of insulin-like growth factors and their receptors, over a time course of several days, in response to hypoxic/ischemic insult to developing or adult brain. The current study tested whether birth insults involving hypoxia may produce long term changes in brain insulin-like growth factor or insulin receptor levels, lasting into adulthood. For this, rats were born vaginally (controls), by cesarean section, or by cesarean section with 15 min of added global anoxia (cesarean section+anoxia), and brain [125I]insulin-like growth factor-I, [125I]insulin-like growth factor-II and [125I]insulin receptor binding sites were assessed autoradiographically at adulthood. [125I]Insulin-like growth factor-I receptor binding sites were increased in all hippocampal subfields (CA1-CA3, dentate gyrus) in rats born either by cesarean section or by cesarean section+anoxia, compared with vaginal birth. [125I]Insulin-like growth factor-II binding was increased in all hippocampal subfields only in rats born by cesarean section+anoxia compared with either vaginal birth or cesarean section groups. [125I]Insulin-like growth factor-I and [125I]insulin-like growth factor-II binding in frontal cortex, striatum and cerebellum were unaffected by birth group, except for increased [125I]insulin-like growth factor-I binding in the cerebellar molecular layer of cesarean-sectioned animals. Birth group had no significant effect on [125I]insulin binding in any brain region. Affinity cross-linking experiments performed with hippocampal membranes from the three birth groups showed that i) [125I]insulin-like growth factor-I and [125I]insulin-like growth factor-II recognized bands of molecular weights characteristic of insulin-like growth factor-I and insulin-like growth factor-II receptors, respectively, and ii) [125I]insulin-like growth factor-I and [125I]insulin-like growth factor-II were displaced more potently by their respective unlabeled ligands than by related molecules. It is concluded that birth insults involving hypoxia can induce lasting increases in insulin-like growth factor-I and -II receptors in the CNS. There is specificity with respect to the subtype of insulin-like growth factor receptor affected by the particular birth insult and the brain region affected. It is suggested that enduring increases in levels of insulin-like growth factor receptors consequent to hypoxic birth insult may help to maintain hippocampal function at adulthood, and could modulate responsiveness to insulin-like growth factor administration.     

Expression of insulin-like growth factor 1 receptor in primary breast cancer: immunohistochemical analysis

Insulin-like growth factor-1 receptor (IGF-1R) has been implicated in regulation in tumor growth. The results of previous studies performed by radioimmunoassay are conflicting, and the prognostic significance of IGF-1R expression in primary breast cancer is still controversial. IGF-1R expression was evaluated in formalin-fixed, paraffin-embedded tissue of 210 primary breast cancer patients by using anti-IGF-1R antibody. The clinicopathologic variables and 5-year disease-free survival were studied, and their correlations between IGF-1R expressions were investigated. IGF-1R overexpression was observed in 43.8% of tumors. IGF-1R overexpression had no correlation with prognosis or with other clinicopathologic parameters, such as age, tumor size, nodal status, histologic grade, hormone receptor status, and human epidermal growth factor 2 status. Though its prognostic value in breast cancer is limited, immunohistochemical evaluation of IGF-1R by using this monoclonal antibody may be useful in translational research using archived material.     

罗格列酮对多囊卵巢综合征患者卵巢黄素化颗粒细胞胰岛素受体底物1和2蛋白表达及酪氨酸磷酸化的影响

目的： 研究罗格列酮对多囊卵巢综合征(PCOS)患者卵巢黄素化颗粒细胞胰岛素受体底物-1(IRS-1)和IRS-2蛋白表达及酪氨酸磷酸化的影响。探讨罗格列酮改善PCOS卵巢局部胰岛素抵抗的作用。方法: 收集行IVF-ET治疗的11例PCOS患者（PCOS组）和15例排卵正常患输卵管性不孕患者（对照组）促排卵后黄素化颗粒细胞行体外培养，分别用不同浓度罗格列酮（0、1、10、100、1 000、10 000 nmol/L）处理细胞48 h，采用RT-PCR、免疫印迹（Western blotting）及免疫沉淀法分别检测卵巢黄素化颗粒细胞IRS-1和IRS-2mRNA的表达、蛋白含量及酪氨酸磷酸化水平。结果: （1）与对照比较，PCOS组黄素化颗粒细胞IRS-1mRNA表达及蛋白含量显著增加（P<0.05），IRS-2mRNA表达及蛋白含量显著降低（P<0.05），IRS-1和IRS-2酪氨酸磷酸化水平均显著降低（P<0.05，P<0.05）；（2）不同浓度罗格列酮作用后，PCOS组黄素化颗粒细胞IRS-1mRNA及蛋白表达显著降低，IRS-2mRNA及蛋白表达显著增加，同时IRS-1和IRS-2酪氨酸磷酸化水平也显著增加，而正常对照组黄素化颗粒细胞IRS表达及酪氨酸磷酸化水平无显著变化。结论: PCOS患者卵巢局部存在胰岛素抵抗，其原因可能与IRS-1和IRS-2蛋白表达及酪氨酸磷酸化异常有关；罗格列酮可以通过调整IRS-1和IRS-2表达失衡，提高IRS-1和IRS-2酪氨酸磷酸化水平，改善PCOS患者卵巢局部胰岛素抵抗。     

Insulin and insulin-like growth factor (IGF I) modulate the effects of bTSH on3H-thymidine incorporation in human thyroid cells in primary culture

Summary The role of TSH in thyroid cell growth and the pathogenesis of goiter has become a matter of recent debate, since many investigators have failed to demonstrate a growth-promoting effect of TSH in human thyroid cells in culture. While those studies have focused on the action of TSH in human thyroid cells, the influence of assay conditions and cofactors has received scant attention. In the present study, we have therefore undertaken to elucidate the effects of insulin and insulin-like growth factor (IGF I) on³H-thymidine uptake in human thyroid cells, particularly with respect to their relation to the actions of bTSH. We could demonstrate a considerable, dose-dependent stimulation of³H-thymidine incorporation in the cells by bTSH that was dependent on the presence of insulin or IGF I; bTSH alone was ineffective in that respect. The concentrations of insulin and IGF I required to facilitate the TSH response were of a magnitude at which both peptides were totally ineffective by themselves. At concentrations of insulin or IGF I that produced a maximum stimulation of³H-thymidine incorporation, the addition of bTSH did result in a slight decrease rather than a further increase of that stimulation. We conclude from these findings, first, that TSH appears to be a growth factor for human thyroid cells under the conditions described, and, second, the effects of TSH on thyroid cell proliferation are under the control of cofactors like insulin and IGF I.Abbreviations bTSH Bovine thyroid stimulating hormone - IGF I Insulin-like growth factor I     

Growth hormone secretion is impaired but not related to insulin sensitivity in non-obese patients with polycystic ovary syndrome

BACKGROUND: The aim of the study was to elucidate the relationship between growth hormone (GH) secretion and insulin resistance in polycystic ovary syndrome (PCOS) patients. In order to exclude the influence of obesity on these parameters, only non-obese PCOS patients were studied. METHODS: Eleven PCOS patients and 11 controls with a body mass index (BMI) 相似文献   

大肠息肉和大肠癌中胰岛素样生长因子Ⅰ受体的表达及其意义

目的 研究胰岛素样生长因子Ⅰ受体(IGF-Ⅰ R)在大肠息肉和大肠癌中的表达及其意义.方法 搜集内镜黏膜切除术(EMR)或内镜黏膜下剥离术(ESD)完整切除并经病理证实的32例患者的共47个大肠息肉,包括炎性息肉、管状腺瘤、绒毛状腺瘤;另选12例正常结肠黏膜组织及20例结肠腺癌黏膜组织作为对照.用免疫组织化学方法检测IGF-Ⅰ R的表达,分析IGF-Ⅰ R的表达程度及其与大肠癌的相关性.结果 IGF-Ⅰ R在正常对照组、炎性息肉组、管状腺瘤组、绒毛状腺瘤组和大肠癌组5组病例间经Spearman双变量等级相关性分析,相关系数为0.574,差异有统计学意义(P<0.01).结论 IGF-Ⅰ R在正常组织、炎性息肉、管状腺瘤、绒毛状腺瘤、大肠癌中的表达依次增加.IGF-Ⅰ R在评价息肉处于黏膜增生-腺瘤-癌变的发展中起了重要的作用.