TY - JOUR
T1 - Alteration of endothelial function markers in women with gestational diabetes and their fetuses
AU - Mordwinkin, Nicholas M.
AU - Ouzounian, Joseph G.
AU - Yedigarova, Larisa
AU - Montoro, Martin N.
AU - Louie, Stan G.
AU - Rodgers, Kathleen E.
N1 - Funding Information:
Declaration of Interest: This study was funded by the National Institutes of Health (Grant Number 5R01HL082722-02). Seed funding was also provided by Department of Obstetrics and Gynecology, Keck School of Medicine, University of Southern California.
PY - 2013/3
Y1 - 2013/3
N2 - Objective: We tested the hypothesis that women with gestational diabetes mellitus (GDM) and their fetuses would demonstrate alterations in markers of endothelial nitric oxide synthase (eNOS) uncoupling, oxidative stress, and endothelial dysfunction and these changes would correlate with the levels of hyperglycemia through a pilot observational case-control study of women with GDM and their fetuses. Methods: Levels of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), C-reactive protein (CRP), nitric oxide (NO), eNOS, p22-phox, and SOD gene expression, and endothelial progenitor cells (EPC) counts in both maternal and cord blood were measured at the time of delivery in women with and without GDM. Results: We demonstrated the presence of decreased maternal circulating EPC counts, increased soluble adhesion molecules in maternal blood, decreased SOD expression in both maternal and cord blood and increased eNOS expression in both maternal and cord blood in women with GDM. Conclusions: These data suggest that the molecular mechanisms behind oxidative stress in women with GDM and their fetuses appear similar to those hypothesized for non-pregnant adults with type 2 diabetes mellitus (DM).
AB - Objective: We tested the hypothesis that women with gestational diabetes mellitus (GDM) and their fetuses would demonstrate alterations in markers of endothelial nitric oxide synthase (eNOS) uncoupling, oxidative stress, and endothelial dysfunction and these changes would correlate with the levels of hyperglycemia through a pilot observational case-control study of women with GDM and their fetuses. Methods: Levels of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), C-reactive protein (CRP), nitric oxide (NO), eNOS, p22-phox, and SOD gene expression, and endothelial progenitor cells (EPC) counts in both maternal and cord blood were measured at the time of delivery in women with and without GDM. Results: We demonstrated the presence of decreased maternal circulating EPC counts, increased soluble adhesion molecules in maternal blood, decreased SOD expression in both maternal and cord blood and increased eNOS expression in both maternal and cord blood in women with GDM. Conclusions: These data suggest that the molecular mechanisms behind oxidative stress in women with GDM and their fetuses appear similar to those hypothesized for non-pregnant adults with type 2 diabetes mellitus (DM).
KW - Endothelial dysfunction
KW - Gestational diabetes mellitus
KW - Oxidative stress
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U2 - 10.3109/14767058.2012.736564
DO - 10.3109/14767058.2012.736564
M3 - Article
C2 - 23046386
AN - SCOPUS:84874089235
SN - 1476-7058
VL - 26
SP - 507
EP - 512
JO - Journal of Maternal-Fetal and Neonatal Medicine
JF - Journal of Maternal-Fetal and Neonatal Medicine
IS - 5
ER -