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Submitted on September 1, 2005
Accepted on November 28, 2005
Department of Molecular Pathology, Molecular Medicine Unit, Royal Free and University College Medical School, London, United Kingdom; College of Medicine and Medical Sciences, Arabian Gulf University, Manama, Kingdom of Bahrain; Department of Molecular Pathology, Molecular Medicine Unit, Royal Free and University College Medical School, London, United Kingdom; Department of Molecular Pathology, Molecular Medicine Unit, Royal Free and University College Medical School, London, United Kingdom; Department of Obstetrics and Gynaecology, University of Bari, Bari, Italy; Department of Obstetrics and Gynaecology, Royal Free and University College Medical School, London, United Kingdom; Department of Molecular Pathology, Molecular Medicine Unit, Royal Free and University College Medical School, London, United Kingdom
* To whom correspondence should be addressed. E-mail: marco.scioscia{at}tin.it.
Context. Preeclampsia is a severe complication of human pregnancy often associated with maternal risk factors. Insulin resistance represents a major risk for developing preeclampsia during pregnancy.
Objective. A putative second messenger of insulin, inositolphosphoglycan P-type (P-IPG), was previously shown to be highly increased during active preeclampsia. Its association with insulin resistance was investigated.
Design and setting. A cross sectional study was carried out in a referral center.
Patients. Nine preeclamptic and eighteen healthy women were recruited and matched for maternal age, BMI, parity, and ethnicity in a 1:2 ratio. Placental specimens were collected immediately after delivery.
Intervention. Placental tissue was incubated with insulin and P-IPG production assessed. Insulin signaling proteins were subsequently studied by immunoblotting.
Results. P-IPG extracted from human term placentas upon incubation with insulin was found to be far lower in preeclampsia than controls (P < 0.001). Immunoblotting studies revealed serine phosphorylation of IRS1 and IRS2 in preeclamptic placentas (P < 0.001) with downstream impairment of insulin signaling. The activation of the p85 regulatory subunit of PI3 Kinase was markedly decreased in preeclamptic samples (P < 0.001).
Conclusions. These findings highlight the importance of P-IPG in active preeclampsia and demonstrate a substantially different response to the insulin stimulus of human preeclamptic placentas. Acquired alterations in activation of proteins involved in insulin signaling may play a role in the complex pathogenesis of preeclampsia probably as a consequence of the immunological dysfunction that occurs in this syndrome. These results seem to confirm an insulin resistant state in preeclamptic placenta and shed a different light on its role in the pathogenesis of this disease with potential therapeutic implications.
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