Neonates from women with pregestational maternal obesity show reduced umbilical vein endothelial response to insulin.
Adult
Arginine
/ metabolism
Case-Control Studies
Endothelial Cells
/ metabolism
Endothelium, Vascular
/ physiopathology
Female
Human Umbilical Vein Endothelial Cells
Humans
Infant, Newborn
Insulin
Insulin Receptor Substrate Proteins
/ metabolism
Myography
Obesity
/ physiopathology
Pregnancy
Pregnancy Complications
/ physiopathology
Primary Cell Culture
Umbilical Veins
/ physiopathology
Young Adult
Endothelium
Insulin resistance
Nitric oxide
Obesity
Placenta
Journal
Placenta
ISSN: 1532-3102
Titre abrégé: Placenta
Pays: Netherlands
ID NLM: 8006349
Informations de publication
Date de publication:
10 2019
10 2019
Historique:
received:
02
04
2019
revised:
09
07
2019
accepted:
15
07
2019
pubmed:
28
7
2019
medline:
25
8
2020
entrez:
27
7
2019
Statut:
ppublish
Résumé
Pregestational maternal obesity (PGMO) associates with foetoplacental vascular endothelial dysfunction and higher risk for insulin resistance in the neonate. We characterised the PGMO consequences on the insulin response of the human foetoplacental vasculature. Umbilical veins were from pregnancies where the mother was with PGMO (body mass index 30-42.3 kg/m Vessel rings from PGMO showed reduced nitric oxide synthase-activity dependent dilation to insulin or calcitonin-gene related peptide compared with PGMN. PGMO associated with higher inhibitor phosphorylation of the insulin receptor substrate 1 (IRS-1) and lower activator phosphorylation of protein kinase B/Akt (Akt). Cells from PGMO also showed lower nitric oxide level and reduced activator serine The lack of response to insulin by the foetoplacental endothelium may result from reduced IRS-1/Akt/eNOS signalling in PGMO. These findings may result in higher risk of insulin resistance in neonates to PGMO pregnancies.
Identifiants
pubmed: 31345420
pii: S0143-4004(19)30517-X
doi: 10.1016/j.placenta.2019.07.007
pii:
doi:
Substances chimiques
IRS1 protein, human
0
Insulin
0
Insulin Receptor Substrate Proteins
0
Arginine
94ZLA3W45F
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
35-44Informations de copyright
Copyright © 2019 Elsevier Ltd. All rights reserved.