Small for Gestational Age and the Metabolic Syndrome: Which Mechanism Is Suggested by Epidemiological and Clinical Studies?

Vol. 65, Suppl. 3, 2006

Free Abstract Article (Fulltext) Article (PDF 229 KB)

Understanding the Biology and Therapeutic Consequences of Being Born SGA.
Editor(s): Czernichow, P. (Paris), Dunger, D. (Cambridge), Lévy-Marchal, C. (Paris)

Size at Birth, Postnatal Growth and the Metabolic Syndrome

Small for Gestational Age and the Metabolic Syndrome: Which Mechanism Is Suggested by Epidemiological and Clinical Studies?
C. Lévy-Marchal, P. Czernichow

INSERM Units 457 and 690, Robert Debré Hospital, Paris, France

Address of Corresponding Author

Horm Res 2006;65 (Suppl. 3):123-130 (DOI: 10.1159/000091517)

Key Words

Adipose tissue
Catch-up growth
Insulin resistance
Intrauterine growth retardation
Type 2 diabetes

Abstract

The metabolic and cardiovascular complications associated with in-utero undernutrition have been identified during the past 10 years. Reduced fetal growth is independently associated with an increased risk of development of cardiovascular diseases, the insulin-resistance syndrome or one of its components (i.e., hypertension, dyslipidaemia, impaired glucose tolerance and type 2 diabetes). Insulin resistance appears to be a key component underlying these metabolic complications. Although the mechanism remains unclear, several pieces of evidence support an active role of adipose tissue in the emergence of insulin resistance (an abnormal growth pattern and repartition, hypersensitivity to catecholamines, regulation of leptin and adiponectin secretion and modulation of peroxisome proliferator-activated receptor gamma ). Among individuals born SGA, those who are more at risk of gaining excess adiposity are those who are thin at birth following a period of fetal growth restriction. This period of undernutrition is followed by a neonatal period of catch-up growth and renutrition. This pattern induces important modifications in adipose tissue, with long-term consequences, among which is a high risk of early development of insulin resistance. Not all individuals born SGA will show such modifications in adipose tissue, meaning that not all of those born SGA are at risk of insulin resistance and diabetes. From a broader point of view, several hypotheses have been proposed over the past 10 years to explain this unexpected association between being born SGA and the later development of disease. Each of them points to a detrimental fetal environment, to a genetic susceptibility or to interactions between these two components playing a critical role in this context. Although not confirmed, the hypothesis suggesting that this association could be the consequence of genetic/environmental interactions remains the most attractive.

Author Contacts

C. Lévy-Marchal
Unité 690 INSERM
Hôpital Robert Debré, 48 Boulevard Sérurier
FR-75935 Paris Cedex 19 (France)
Tel. +33 1 4003 2355, Fax +33 1 4040 9195, E-Mail clairelm@rdebre.inserm.fr

Article Information

Published online: April 10, 2006
Number of Print Pages : 8
Number of Figures : 4, Number of Tables : 0, Number of References : 31

Medline Abstract (ID 16612125)

Download Citation

Cited In

Title change 2010 to:

This journal is part of the third subject package of the Karger

Journal Archive Collection

Information on packages (PDF)
Free sample issues

For non-native English speakers and international authors who would like assistance with their writing before submission, we suggest American Journal Experts for their scientific editing service.