Zhang Tao, Fang Min, Fu Zi-Mu, Du He-Chun, Yuan Hua, Xia Gui-Yu, Feng Jie, Yin Gui-Yun
Shaoxing Women and Children's Hospital, Shaoxing 312000, China.
Department of Gynaecology, Linyi People's Hospital, Linyi 276000, China.
Asian Pac J Trop Med. 2014 Apr;7(4):309-12. doi: 10.1016/S1995-7645(14)60045-6.
To analyze the expression of phosphatidylinositol 3 kinase (PI3-K), protein kinase B (PKB) and glycogen synthase kinase 3 beta (GSK-3 β) in skeletal muscle tissue of gestational diabetes mellitus (GDM).
A total of 90 cases of pregnant women were divided into observation group and control group according to the occurrence of GDM with 45 cases in either, and the expression of PI3-K, PKB, GSK-3 β mRNA expression in skeletal muscle tissue was compared between two groups.
The total PI3-K p85 protein was significantly higher in the observation group compared with the control group, the activity of PI3-K was lower than that of the latter; The total PKB, GSK-3 β protein in skeletal tissue had no significant difference between two groups, while the serine phosphorylation levels of PKB and GSK-3β were significantly lower in observation group compared with the control group.
The downregulation of PI3-K, PKB and GSK-3βin skeletal tissue of GDM caused by phosphorylation dysfunction of signaling molecules is the reason for insulin resistance and transporter function decline which lead to GDM.
分析磷脂酰肌醇3激酶（PI3-K）、蛋白激酶B（PKB）和糖原合酶激酶3β（GSK-3β）在妊娠期糖尿病（GDM）骨骼肌组织中的表达。
将90例孕妇根据是否发生GDM分为观察组和对照组，每组45例，比较两组骨骼肌组织中PI3-K、PKB、GSK-3β mRNA的表达。
观察组PI3-K p85总蛋白较对照组显著升高，PI3-K活性低于对照组；两组骨骼肌组织中PKB、GSK-3β总蛋白无显著差异，而观察组PKB和GSK-3β的丝氨酸磷酸化水平较对照组显著降低。
信号分子磷酸化功能障碍导致GDM患者骨骼肌组织中PI3-K、PKB和GSK-3β下调，是导致胰岛素抵抗和转运功能下降进而引发GDM的原因。
