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The developmental origins of insulin resistance

The developmental origins of insulin resistance
The developmental origins of insulin resistance
Until recently, the principal causes of degenerative disease were thought to act in adult life and to accelerate destructive processes, such as the formation of atheroma and rise in blood pressure. Recent observations that people who develop coronary heart disease grow differently to other people during fetal life and childhood have, however, led to a new 'developmental' model for the disease. Low birthweight has been shown to be associated with increased rates of coronary heart disease, type 2 diabetes mellitus and altered glucose tolerance. These associations with low birthweight extend across the normal range of birthweight and reflect slow fetal growth rather than premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations suggest that low birthweight, thinness at 2 years of age and an increase in body mass index (BMI) after the age of 2 years are each associated with the development of insulin resistance in later life. The prevention of a substantial proportion of type 2 diabetes and other disorders linked to insulin resistance may, therefore, depend on interventions during development. These include protecting the growth of babies during the first 2 years after birth by good infant feeding practices and preventing a rapid increase in BMI after the age of 2 years. Improving fetal nutrition remains an important long-term goal.
fetal growth, childhood growth, insulin resistance, type 2 diabetes mellitus, body mass index
0301-0163
2-7
Barker, David J.P.
5c773838-b094-4ac1-999b-b5869717f243
Barker, David J.P.
5c773838-b094-4ac1-999b-b5869717f243

Barker, David J.P. (2005) The developmental origins of insulin resistance. Hormone Research, 64 (3), 2-7. (doi:10.1159/10.1159/000089311).

Record type: Article

Abstract

Until recently, the principal causes of degenerative disease were thought to act in adult life and to accelerate destructive processes, such as the formation of atheroma and rise in blood pressure. Recent observations that people who develop coronary heart disease grow differently to other people during fetal life and childhood have, however, led to a new 'developmental' model for the disease. Low birthweight has been shown to be associated with increased rates of coronary heart disease, type 2 diabetes mellitus and altered glucose tolerance. These associations with low birthweight extend across the normal range of birthweight and reflect slow fetal growth rather than premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations suggest that low birthweight, thinness at 2 years of age and an increase in body mass index (BMI) after the age of 2 years are each associated with the development of insulin resistance in later life. The prevention of a substantial proportion of type 2 diabetes and other disorders linked to insulin resistance may, therefore, depend on interventions during development. These include protecting the growth of babies during the first 2 years after birth by good infant feeding practices and preventing a rapid increase in BMI after the age of 2 years. Improving fetal nutrition remains an important long-term goal.

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More information

Published date: 2005
Keywords: fetal growth, childhood growth, insulin resistance, type 2 diabetes mellitus, body mass index

Identifiers

Local EPrints ID: 25242
URI: http://eprints.soton.ac.uk/id/eprint/25242
ISSN: 0301-0163
PURE UUID: 31bdf2bb-ceaf-4117-8465-22823b18e748

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Date deposited: 07 Apr 2006
Last modified: 15 Jul 2019 19:16

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