当前位置:主页 > 医学论文 > 妇产科论文 >

妊娠期糖尿病患者胎盘组织胰岛素受体底物1、蛋白酪氨酸磷酸酶1B表达及意义

发布时间:2019-07-06 18:16
【摘要】:目的探讨妊娠期糖尿病(GDM)患者胎盘组织胰岛素受体底物1(IRS-1)、蛋白酪氨酸磷酸酶1B(PTP1B)表达及意义。方法选择GDM孕妇49例(GDM组),正常足月妊娠孕妇50例(正常组)。两组均于孕24~28周检测空腹胰岛素(FINS)、空腹血糖(FPG),采用胰岛素稳态模型评估法(HOMA)计算胰岛素抵抗指数(HOMAIR)、胰岛β细胞功能(HOMA-β%)、胰岛素敏感指数(HOMA-ISI);两组分娩后取胎盘组织,采用免疫组化ABC法检测胎盘组织IRS-1、PTP 1B。结果 GDM组FPG、FINS、HOMA-IR均高于正常组(P均0.01),HOMA-ISI、HOMA-β%均低于正常组(P均0.01)。正常组胎盘组织IRS-1阳性表达率为100%,GDM组为63.26%,两组比较P0.01。正常组胎盘组织PTP 1B阳性表达率为56.00%,GDM组为91.83%,两组比较P0.01。GDM患者胎盘组织PTP 1B与IRS-1表达呈负相关(r=-4.85,P0.01);IRS-1与HOMA-IR呈负相关(r=-0.552,P0.01),与HOMA-β%和HOMA-ISI无相关性(P均0.05);PTP 1B与HOMA-IR呈正相关(r=0.563,P0.01),与HOMA-β%和HOMA-ISI无相关性(P均0.05)。结论 GDM患者胎盘组织IRS-1表达降低,PTP 1B表达升高,且均与HOMA-IR相关;胰岛素信号传导系统中信号蛋白表达异常可能与GDM发病有关。
[Abstract]:Objective to investigate the expression and significance of insulin receptor substrate 1 (IRS-1) and protein tyrosine phosphatase 1B (PTP1B) in placenta of patients with gestational diabetes mellitus (GDM). Methods 49 GDM pregnant women (GDM group) and 50 normal term pregnant women (normal group) were selected. Fasting insulin (FINS), fasting blood glucose (FPG), was measured at 24 脳 28 weeks of gestation. Insulin homeostasis model (HOMA) was used to calculate insulin resistance index (HOMAIR), islet 尾 cell function (HOMA- 尾%) and insulin sensitivity index (HOMA-ISI). Placental tissues were taken after delivery and placental tissue IRS-1,PTP 1B was detected by ABC method. Results FPG,FINS,HOMA-IR in GDM group was higher than that in normal group (P < 0.01), and HOMA-ISI,HOMA- 尾% was lower than that in normal group (P < 0.01). The positive expression rate of IRS-1 in placenta was 100% in normal group and 63.26% in GDM group. The positive expression rate of PTP 1B in placenta of normal group was 56.00%, and that of GDM group was 41.83%. There was a negative correlation between PTP 1B and IRS-1 expression in placenta of P0.01.GDM patients (r 鈮,

本文编号:2511240

资料下载
论文发表

本文链接:https://www.wllwen.com/yixuelunwen/fuchankeerkelunwen/2511240.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户e9701***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com