Effects of gestational diabetes mellitus on proteins implicated in insulin signaling in human placenta

被引:50
作者
Alonso, Ana
Del Rey, Carmen Gonzalez
Navarro, Ana
Tolivia, Jorge
Gonzalez, Celestino G.
机构
[1] Univ Oviedo, Dept Funct Biol, Physiol Area, E-33006 Oviedo, Spain
[2] Virgen De La Concha Hosp, Dept Pathol, Zamora, Spain
[3] Univ Oviedo, Dept Morphol & Cellular Biol, Oviedo, Spain
关键词
placenta; gestational diabetes mellitus; insulin receptor; insulin receptor substrate-1; leptin receptor; estrogen receptor; p85; alpha;
D O I
10.1080/09513590600921374
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
Objective. Placenta plays a central role in fetal nutrition. During gestational diabetes mellitus (GDM), it suffers structural and functional alterations which affect the health of both mother and fetus. In the present study we aimed to clarify if GDM modifies the amounts of leptin receptor (Ob-R) and of the main proteins implicated in insulin signal transmission (insulin receptor, insulin receptor substrate-1 and phosphatidylinositol-3-kinase subunit p85 alpha) in human placenta; we also attempted to confirm the presence of estrogen receptor-x to determine the effect of GDM on its amount. Methods. Placentas were recovered from 30 women with uncomplicated pregnancies and 20 women who developed GDM. Western blotting and immunocytochemistry experiments were performed to investigate the above-mentioned proteins. Results. We observed that all proteins studied were increased in GDM. However, it is unknown if this is a consequence of GDM or the result of medical treatments used to mitigate the injurious effects of GDM. Conclusions. Probably, the changes we found are indicative of the protective role of the placenta prior to the injurious effects of GDM and/or an important indicator of placental aging. Some aspects related to the link between non-genomic estrogen action, the mitogenic action of insulin and the role of Ob-R in placenta from normal and GDM women need to be investigated in greater depth.
引用
收藏
页码:526 / 535
页数:10
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