Diabetes
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Radaelli, T.
Right arrow Articles by Hauguel-de Mouzon, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Radaelli, T.
Right arrow Articles by Hauguel-de Mouzon, S.
Social Bookmarking
 Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes 52:2951-2958, 2003
© 2003 by the American Diabetes Association, Inc.

Gestational Diabetes Induces Placental Genes for Chronic Stress and Inflammatory Pathways

Tatjana Radaelli, Ali Varastehpour, Patrick Catalano, and Sylvie Hauguel-de Mouzon

From the Department of Reproductive Biology, Schwartz Center for Metabolism and Nutrition, University School of Medicine at MetroHealth Medical Center, Case Western Reserve University, Cleveland, Ohio

A physiological state of insulin resistance is required to preferentially direct maternal nutrients toward the feto-placental unit, allowing adequate growth of the fetus. When women develop gestational diabetes mellitus (GDM), insulin resistance is more severe and disrupts the intrauterine milieu, resulting in accelerated fetal development with increased risk of macrosomia. As a natural interface between mother and fetus, the placenta is the obligatory target of such environmental changes. However, the molecular basis for the imbalance that leads to fetal, neonatal, and adult metabolic compromises is not well understood. We report that GDM elicits major changes in the expression profile of placental genes with a prominent increase in markers and mediators of inflammation. Within the 435 transcripts reproducibly modified, genes for stress-activated and inflammatory responses represented the largest functional cluster (18.5% of regulated genes). Upregulation of interleukins, leptin, and tumor necrosis factor-{alpha} receptors and their downstream molecular adaptors indicated an activation of pathways recruiting stress-activated protein/c-Jun NH2-terminal kinases. Transcriptional activation of extracellular matrix components and angiogenic activators pointed to a major structural reorganization of the placenta. Thus, placental transcriptome emerges as a primary target of the altered environment of diabetic pregnancy. The genes identified provide the basis to elucidate links between inflammatory pathways and GDM-associated insulin resistance.


Address correspondence and reprint requests to Dr. Sylvie Hauguel-de Mouzon, Department of Obstetrics, 2500 MetroHealth Dr., Cleveland, OH 44109. E-mail: sdemouzon{at}aol.com


Add to CiteULike CiteULike   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
DiabetesHome page
S. M. Nelson, N. Sattar, D. J. Freeman, J. D. Walker, and R. S. Lindsay
Inflammation and Endothelial Activation Is Evident at Birth in Offspring of Mothers With Type 1 Diabetes
Diabetes, November 1, 2007; 56(11): 2697 - 2704.
[Abstract] [Full Text] [PDF]


Home page
Diabetes CareHome page
G. Desoye and S. Hauguel-de Mouzon
The Human Placenta in Gestational Diabetes Mellitus: The insulin and cytokine network
Diabetes Care, July 1, 2007; 30(Supplement_2): S120 - S126.
[Full Text] [PDF]


Home page
Reproductive SciencesHome page
S. Lambin, R. van Bree,, I. Vergote, and J. Verhaeghe
Chronic Tumor Necrosis Factor-{alpha} Infusion in Gravid C57BL6/J Mice Accelerates Adipose Tissue Development in Female Offspring
Reproductive Sciences, December 1, 2006; 13(8): 558 - 565.
[Abstract] [PDF]


Home page
HeartHome page
L K Hornberger
Maternal diabetes and the fetal heart
Heart, August 1, 2006; 92(8): 1019 - 1021.
[Abstract] [Full Text] [PDF]


Home page
Biol. Reprod.Home page
M. C. Henson and V. D. Castracane
Leptin in Pregnancy: An Update
Biol Reprod, February 1, 2006; 74(2): 218 - 229.
[Abstract] [Full Text] [PDF]


Home page
Reproductive SciencesHome page
T. Radaelli, J. Uvena-Celebrezze, J. Minium, L. Huston-Presley, P. Catalano, and S. Hauguel-de Mouzon
Maternal Interleukin-6: Marker of Fetal Growth and Adiposity
Reproductive Sciences, January 1, 2006; 13(1): 53 - 57.
[Abstract] [PDF]


Home page
J. Clin. Endocrinol. Metab.Home page
A. Varastehpour, T. Radaelli, J. Minium, H. Ortega, E. Herrera, P. Catalano, and S. Hauguel-de Mouzon
Activation of Phospholipase A2 Is Associated with Generation of Placental Lipid Signals and Fetal Obesity
J. Clin. Endocrinol. Metab., January 1, 2006; 91(1): 248 - 255.
[Abstract] [Full Text] [PDF]


Home page
Reproductive SciencesHome page
J. Verhaeghe, R. van Bree, S. Lambin, and S. Caluwaerts
Adipokine Profile and C-Reactive Protein in Pregnancy: Effects of Glucose Challenge Response Versus Body Mass Index
Reproductive Sciences, July 1, 2005; 12(5): 330 - 334.
[Abstract] [PDF]


Home page
J. Clin. Endocrinol. Metab.Home page
A. Megia, L. Gallart, J.-M. Fernandez-Real, J. Vendrell, I. Simon, C. Gutierrez, and C. Richart
Mannose-Binding Lectin Gene Polymorphisms Are Associated with Gestational Diabetes Mellitus
J. Clin. Endocrinol. Metab., October 1, 2004; 89(10): 5081 - 5087.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 2003 by the American Diabetes Association.