Fetal origins of adult disease: a paediatric perspective
- PMID: 16311944
- DOI: 10.1007/s11154-005-6184-0
Fetal origins of adult disease: a paediatric perspective
Abstract
Prepubertal children born SGA or VLBW premature exhibit marked insulin resistance. There are similarities between SGA and VLBW children in that both are exposed to sub-optimal environments that encompass undernutrition and/or malnutrition during the equivalent of the last trimester of pregnancy. Although both SGA and VLBW groups fail to reach genetic height potential and are recognized causes of short stature in childhood, there are differences between the groups with respect to the growth hormone and IGF-I axis.SGA children have elevated IGFI levels, possibly due to either hyperinsulinism or partial IGF-I resistance, whereas VLBW children have low IGF-I and IGFBP-3 levels suggestive of GH resistance. Thus the nature and timing of the early insult may lead to discordant changes to the metabolic and endocrine axes.IVF children are taller with increased IGF I, IGF II and IGFBP3 expression. These changes could be due to alterations in the environment of the periconceptual embryo resulting in changes in imprinting of genes involved in growth and development. The phenotypic, endocrine and metabolic consequences of alterations in the periconceptual, fetal and early neonatal periods is an area of intense investigation. Future research in this field is likely to focus on the mechanisms through which environmental changes lead to these programmed effects.
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