Low birth weight: effect on insulin sensitivity and lipid metabolism
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Updated: Sep 27, 2026

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)
Published on: January 7, 2018
Delphine Jaquet1, Jaquet Léger, Claire Lévy-Marchal
1INSERM Unité 457, Hôpital Robert Debré, Paris, France.
Insights
Reduced fetal growth is linked to metabolic and cardiovascular issues like insulin resistance and type 2 diabetes. Genetic and environmental factors likely interact to cause these complications.
Area of Science:
- Metabolic and Cardiovascular Health
- Developmental Origins of Health and Disease (DOHaD)
Background:
- Reduced fetal growth is increasingly recognized as a precursor to metabolic and cardiovascular complications.
- These complications include insulin resistance syndrome (dyslipidemia, impaired glucose tolerance, type 2 diabetes) and cardiovascular diseases.
Purpose of the Study:
- To explore the association between reduced fetal growth and metabolic/cardiovascular complications.
- To investigate the underlying mechanisms, particularly the role of insulin resistance and adipose tissue.
Main Methods:
- Review of existing literature over the past 10 years.
- Analysis of proposed hypotheses regarding the etiology of these complications.
Main Results:
- Insulin resistance appears to be a primary driver of these complications.
- The link between reduced fetal growth and other metabolic syndrome parameters is less consistent.
- Genetic predisposition influences the manifestation and onset age of these conditions.
Conclusions:
- The precise mechanisms linking reduced fetal growth to insulin resistance are still unclear.
- Adipose tissue may play a crucial role in the development of insulin resistance.
- Genetic/environmental interactions are the most compelling hypothesis for this association.
Abstract:
The metabolic and cardiovascular complications associated with reduced fetal growth have been identified during the past 10 years. These complications that encompass cardiovascular diseases and insulin resistance syndrome consist of dyslipidemia, impaired glucose tolerance or type 2 diabetes and appear to result from the initial development of insulin resistance. The association of reduced fetal growth with the other parameters of the syndrome X appear less constant than with insulin resistance and the expression and/or the age of onset seem to depend on the degree of genetic predisposition of the population. Although the mechanisms underlying the development of the insulin resistance associated with reduced fetal growth remain unclear, some evidence argues in favor of a key role of the adipose tissue. Several hypotheses have been proposed over the past 10 years to understand this unexpected association. Each of them points to either a detrimental fetal environment or genetic susceptibilities or interactions between these two components as 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 at the moment the most attractive.
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