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Diabetologia. 2005 May;48(5):849-55. Epub 2005 Apr 15.

Dynamic change in adiposity from fetal to postnatal life is involved in the metabolic syndrome associated with reduced fetal growth.

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  • 1INSERM Unit 690, Hôpital Robert Debré, 48 Boulevard Sérurier, 75019 Paris, France.



The aims of this study were to establish the role of insulin resistance in the metabolic syndrome associated with restricted fetal growth and to characterise the fetal and postnatal determinants responsible for the long-term metabolic outcome.


The study population consisted of adults selected on birth data from a maternity registry and born either small for gestational age (SGA) (n=734, birthweight<tenth percentile) or appropriate for gestational age (AGA) (n=886, 25th<birthweight<75th percentile) and in whom clinical and metabolic parameters of the metabolic syndrome were measured at 22 years of age.


Mean values of all components of the metabolic syndrome significantly differed between the two groups, with the metabolic syndrome observed in 2.3% of the SGA group and in 4 per thousand of the AGA group (p=0.0004). In SGA subjects, the upper tertile of fasting insulinaemia was associated with the highest values of systolic (p=0.001) and diastolic (p=0.02) blood pressure, triglyceridaemia (p=0.005) and glycaemia at fasting (p=0.0001) and during OGTT (p=0.0001). In SGA subjects, insulin resistance was not related to birthweight itself (p=0.26), but correlated negatively with BMI at birth (p=0.03) and positively with the subsequent postnatal catch-up in BMI (p=0.009).


Insulin resistance is the keystone of metabolic syndrome associated with SGA, and its origin should be sought in the fetal development process of adiposity that is responsible for postnatal growth and the later development of insulin resistance.

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