Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/66307
Citations
Scopus Web of Science® Altmetric
?
?
Type: Journal article
Title: Fetal growth restriction, catch-up growth and the early origins of insulin resistance and visceral obesity
Author: Morrison, J.
Duffield, J.
Muhlhausler, B.
Gentili, S.
McMillen, I.
Citation: Pediatric Nephrology, 2010; 25(4):669-677
Publisher: Springer-Verlag
Issue Date: 2010
ISSN: 0931-041X
1432-198X
Statement of
Responsibility: 
Janna L. Morrison, Jaime A. Duffield, Beverly S. Muhlhausler, Sheridan Gentili, Isabella C. McMillen
Abstract: There is an association between growing slowly before birth, accelerated growth in early postnatal life and the emergence of insulin resistance, visceral obesity and glucose intolerance in adult life. In this review we consider the pathway through which intrauterine growth restriction (IUGR) leads to the initial increase in insulin sensitivity and to catch-up growth. We also discuss the importance of the early insulin environment in determining later visceral adiposity and the intrahepatic mechanisms that may result in the emergence of glucose intolerance in a subset of IUGR infants. We present evidence that a key fetal adaptation to poor fetal nutrition is an upregulation of the abundance of the insulin receptor in the absence of an upregulation of insulin signalling in fetal skeletal muscle. After birth, however, there is an upregulation in the abundance of the insulin receptor and the insulin signalling pathway in the IUGR offspring. Thus, the origins of the accelerated postnatal growth rate experienced by IUGR infants lie in the fetal adaptations to a poor nutrient supply. We also discuss how the intracellular availability of free fatty acids and glucose within the visceral adipocyte and hepatocyte in fetal and neonatal life are critical in determining the subsequent metabolic phenotype of the IUGR offspring. It is clear that a better understanding of the relative contributions of the fetal and neonatal nutrient environment to the regulation of key insulin signalling pathways in muscle, visceral adipose tissue and the liver is required to support the development of evidence-based intervention strategies and better outcomes for the IUGR infant.
Keywords: Fetus; Placenta; IUGR; Insulin; Obesity
Rights: © IPNA 2009
RMID: 0020108839
DOI: 10.1007/s00467-009-1407-3
Appears in Collections:Molecular and Biomedical Science publications

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.