Perinatal programming of adult metabolic homeostasis: Lessons from experimental studies

Kathryn L. Gatford, Miles J. De Blasio, Miodrag Dodic, Dane M. Horton, Karen L. Kind

Research output: Chapter in Book/Report/Conference proceedingChapter (Book)Researchpeer-review

Abstract

Poor fetal growth and associated neonatal catch-up growth are independent risk factors for metabolic disease in later life. Epidemiological studies in humans consistendy 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.

Original languageEnglish
Title of host publicationEarly Life Origins of Health and Disease
EditorsNathan Back
Chapter13
Pages157-176
Number of pages20
DOIs
Publication statusPublished - 1 Dec 2006

Publication series

NameAdvances in Experimental Medicine and Biology
Volume573
ISSN (Print)0065-2598

Cite this