AI Article Synopsis
- The study investigates how insulin affects the expression of aquaporins (AQPs) in fetal membranes of diabetic women during pregnancy, focusing on AQPs 1, 3, 8, and 9.
- Researchers compared fetal membranes from control and diabetic groups using various methods, revealing significant differences in AQP expression, especially lower AQP3 in type 2 diabetes (T2D) and gestational diabetes (GD) cases.
- Findings suggest that insulin can repress AQP3 expression in non-diabetic fetal membranes, a process affected by intracellular signaling pathways, indicating that hyperinsulinism in T2D and GD may lead to reduced AQP3 expression and function.
Article Abstract
Context: During pregnancy, aquaporins (AQPs) expressed in fetal membranes are essential for controlling the homeostasis of the amniotic volume, but their regulation by insulin was never explored in diabetic women.
Objective: The aim of our study was to investigate the involvement of AQPs 1, 3, 8, and 9 expressed in fetal membranes in diabetic parturient women and the control of their expression by insulin.
Design And Participants: From 129 fetal membranes in four populations (controls, type 1, type 2 [T2D], and gestational diabetes [GD]), we established an expression AQP profile. In a second step, the amnion was used to study the control of the expression and functions of AQPs 3 and 9 by insulin.
Main Outcomes And Measures: The expression of transcripts and proteins of AQPs was studied by quantitative RT-PCR and ELISA. We analyzed the regulation by insulin of the expression of AQPs 3 and 9 in the amnion. A tritiated glycerol test enabled us to measure the impact of insulin on the functional characteristics. Using an inhibitor of phosphatidylinositol 3-kinase, we analyzed the insulin intracellular signaling pathway.
Results: The expression of AQP3 protein was significantly weaker in groups T2D and GD. In nondiabetic fetal membranes, we showed for the amnion (but not for the chorion) a significant repression by insulin of the transcriptional expression of AQPs 3 and 9, which was blocked by a phosphatidylinositol 3-kinase inhibitor.
Conclusion: In fetal membranes, the repression of AQP3 protein expression and functions observed in vivo is allowed by the hyperinsulinism described in pregnant women with T2D or GD.
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| http://dx.doi.org/10.1210/jc.2015-2057 | DOI Listing |
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