Medizinische Universität Graz - Research portal

Logo MUG Resarch Portal

Selected Publication:

SHR Neuro Cancer Cardio Lipid Metab Microb

Colomiere, M; Permezel, M; Riley, C; Desoye, G; Lappas, M.
Defective insulin signaling in placenta from pregnancies complicated by gestational diabetes mellitus.
Eur J Endocrinol. 2009; 160(4):567-578 Doi: 10.1530/EJE-09-0031 [OPEN ACCESS]
Web of Science PubMed FullText FullText_MUG Google Scholar

 

Co-authors Med Uni Graz
Desoye Gernot
Altmetrics:

Dimensions Citations:

Plum Analytics:

Scite (citation analytics):

Abstract:
Objective: Studies in adipose tissue and skeletal muscle suggest that impaired insulin action is due to defects in the insulin signaling pathway and may play a role in the pathophysiology of insulin resistance associated with gestational diabetes mellitus (GDM) and obesity. The present study tested the hypothesis that endogenous expression levels in the human term placenta of insulin signaling components are altered in placental tissue from GDM women in comparison with normal controls and maternal obesity Design and methods: Placental tissue was collected from normal, diet-controlled GDM, and insulin-controlled GDM in both non-obese and obese women (n = 6-7 per group). Western blotting and quantitative RT-PCR was performed to determine the level of expression in the insulin signaling pathway. Results: There was a significant increase in insulin receptor (IR) substrate (IRS)-1 protein expression with a Concurrent decrease in IRS-2 protein expression in non-obese women with insulin-controlled GDM compared with diet-controlled GDM and normal controls. Furthermore, a decrease in both protein and mRNA expression of phosphatidyl-inositol-3-kinase (PI3-K) p85 alpha and glucose transporter (GLUT)-4 was observed in non-obese and obese women with insulin controlled GDM compared with normal controls. When comparing non-obese to obese patients, significant decreases in mRNA expression of IR-beta, PI3K p85 alpha and GLUT-4 was found in obese patients. Conclusion: Our results Suggest that. post receptor defects are present in the insulin signaling pathway in placenta of women with pregnancies complicated by diabetes and obesity. In addition, expression Studies derrionstrate post receptor alterations in insulin signaling possibly under selective maternal regulation and not fetal regulation.
Find related publications in this database (using NLM MeSH Indexing)
Adult -
Blotting, Western -
C-Peptide - metabolism
Cell Membrane - metabolism
Cohort Studies -
Diabetes, Gestational - physiopathology
Electrophoresis, Polyacrylamide Gel -
Enzyme-Linked Immunosorbent Assay -
Female -
Glucose - metabolism
Glucose Transporter Type 4 - metabolism
Humans -
Immunohistochemistry -
Indicators and Reagents -
Insulin - physiology
Obesity - complications Obesity - metabolism
Phosphatidylinositol 3-Kinases - metabolism
Placenta - physiopathology
Pregnancy -
RNA, Messenger - biosynthesis RNA, Messenger - genetics
Reverse Transcriptase Polymerase Chain Reaction -
Signal Transduction - physiology

© Med Uni GrazImprint