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Vascular dysfunction in the diabetic placenta: causes and consequences.

Lopa Leach¹, Alice Taylor, Flavia Sciota

¹School of Biomedical Sciences, Centre for Integrated Systems Biology and Medicine, Institute of Clinical Research, Faculty of Medicine and Health Sciences, University of Nottingham, UK. lopa.leach@nottingham.ac.uk

Journal of Anatomy

|July 1, 2009

Summary

Maternal diabetes impacts the human placenta's vascular system, causing increased blood vessel growth and leakiness. Further research is needed to determine if high maternal blood sugar or fetal insulin is the primary cause.

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Area of Science:

Obstetrics and Gynecology
Vascular Biology
Endocrinology

Background:

The fetoplacental vascular system is susceptible to maternal diabetes.
Diabetic conditions can lead to fetal endocrine issues, affecting placental vasculature.
Existing research describes placental vascular changes in Type 1 diabetes, including increased angiogenesis and leakiness.

Purpose of the Study:

To investigate the vascular changes in the human placenta due to maternal diabetes.
To explore the roles of maternal hyperglycemia and fetal hyperinsulinemia in these vascular alterations.
To elucidate the molecular mechanisms underlying placental vascular pathology in diabetes.

Main Methods:

Analysis of placental vascular phenotypes in Type 1 diabetic pregnancies.
Review of mechanistic studies on high glucose and insulin effects on vascular systems.
Discussion of the roles of advanced glycation products and oxidative stress.

Main Results:

Diabetic placentas exhibit increased angiogenesis, altered vessel maturity, and enhanced leakiness.
Elevated placental vascular endothelial growth factor (VEGF) is associated with these vascular changes.
Mechanistic studies indicate high glucose and insulin affect vascular endothelial growth factor, nitric oxide, and protein kinase C, impacting vascular junctions and albumin leakage.

Conclusions:

Maternal diabetes induces significant vascular changes in the human placenta.
The precise contribution of maternal hyperglycemia versus fetal hyperinsulinemia requires further investigation in human placentas.
Altered molecular pathways involving VEGF, nitric oxide, protein kinase C, and advanced glycation products contribute to diabetic placental vascular pathology.