Role of Insulin and Adenosine in the Human Placenta Microvascular and Macrovascular Endothelial Cell Dysfunction in Gestational Diabetes Mellitus

Guzman-Gutierrez, Enrique, Arroyo, Pablo, Salsoso, Rocio, Fuenzalida, Barbara, Saez, Tamara, Leiva, Andrea, Pardo, Fabian and Sobrevia, Luis (2014) Role of Insulin and Adenosine in the Human Placenta Microvascular and Macrovascular Endothelial Cell Dysfunction in Gestational Diabetes Mellitus. Microcirculation, 21 1: 26-37. doi:10.1111/micc.12077


Author Guzman-Gutierrez, Enrique
Arroyo, Pablo
Salsoso, Rocio
Fuenzalida, Barbara
Saez, Tamara
Leiva, Andrea
Pardo, Fabian
Sobrevia, Luis
Title Role of Insulin and Adenosine in the Human Placenta Microvascular and Macrovascular Endothelial Cell Dysfunction in Gestational Diabetes Mellitus
Journal name Microcirculation   Check publisher's open access policy
ISSN 1073-9688
1549-8719
Publication date 2014-01-01
Year available 2014
Sub-type Article (original research)
DOI 10.1111/micc.12077
Open Access Status Not Open Access
Volume 21
Issue 1
Start page 26
End page 37
Total pages 12
Place of publication Chichester, West Sussex, United Kingdom
Publisher John Wiley and Sons Ltd.
Language eng
Subject 1314 Physiology
2737 Physiology (medical)
1312 Molecular Biology
2705 Cardiology and Cardiovascular Medicine
Abstract Microvascular and macrovascular endothelial function maintains vascular reactivity. Several diseases alter endothelial function, including hypertension, obesity, and diabetes mellitus. In addition, micro- and macrovascular endothelial dysfunction is documented in GDM with serious consequences for the growing fetus. Increased l-arginine uptake via hCAT-1 and NO synthesis by eNOS is associated with GDM. These alterations are paralleled by activation of purinergic receptors and increased umbilical vein, but not arteries blood adenosine accumulation. GDM associates with NO-reduced adenosine uptake in placental endothelium, suggested to maintain and/or facilitate insulin vasodilation likely increasing hCAT-1 and eNOS expression and activity. It is proposed that increased umbilical vein blood adenosine concentration in GDM reflects a defective metabolic state of human placenta. In addition, insulin recovers GDM-alterations in hCAT-1 and eNOS in human micro- and macrovascular endothelium, and its biological actions depend on preferential activation of insulin receptors A and B restoring a normal-like from a GDM-like phenotype. We summarized existing evidence for a potential role of insulin/adenosine/micro- and macrovascular endothelial dysfunction in GDM. These mechanisms could be crucial for a better management of the mother, fetus and newborn in GDM pregnancies.
Keyword Arginine membrane transport
Endothelial dysfunction
Nitric oxide
Pregnancy
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: UQ Centre for Clinical Research Publications
Official 2015 Collection
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 21 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 21 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Sun, 26 Jan 2014, 10:10:58 EST by System User on behalf of UQ Centre for Clinical Research