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Type: Journal article
Title: Perinatal programming of adult metabolic homeostasis: Lessons from experimental studies
Author: Gatford, K.
De Blasio, M.
Dodic, M.
Horton, D.
Kind, K.
Citation: Advances in Experimental Medicine and Biology, 2006; 573:157-176
Part of: Advances in Experimental Medicine and Biology ; 573
Publisher: Kluwer Academic / Plenum Publ
Issue Date: 2006
ISSN: 0065-2598
Editor: Wintour, E.M.
Owens, J.A.
Statement of
Kathryn L. Gatford, Miles J. De Blasio, Miodrag Dodic, Dane M. Horton and Karen L. Kind
Abstract: Poor fetal growth and associated neonatal catch-up growth are independent risk factors for metabolic disease in later life. Epidemiological studies in humans consistently show associations of small size at birth and later glucose intolerance and/or diabetes. A primary defect is thought to be insulin resistance, which is associated with both small size at birth and neonatal catch-up growth. The available evidence suggests that this resistance may result from a signalling defect downstream of the insulin receptor in peripheral tissues. Recent evidence also suggests that insulin secretion may be impaired in the individual who was small at birth. Most of the contemporary data in humans relates later outcomes to size at birth rather than to specific exposures. Experimental models that restrict fetal growth or produce variation in size at birth have therefore been used to explore these associations between small size at birth, neonatal catch-up growth and later metabolic disease. In this chapter we will review what has been learnt from human and experimental studies about the mechanistic basis for poor metabolic homeostasis following restricted fetal growth and neonatal catch-up growth, and comment on future directions in this area.
Description: The original publication can be found at
DOI: 10.1007/0-387-32632-4_13
Published version:
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