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Born small for gestational age: increased risk of type 2 diabetes, hypertension and hyperlipidaemia in adulthood
Delphine Jaquet1, Paul Czernichow
1INSERM Unité 457, Hôspital Robert Debré, Paris, France.
Insights
Reduced fetal growth is linked to metabolic and cardiovascular issues like insulin resistance and type 2 diabetes. Genetic-environmental interactions are the leading hypothesis for this connection.
Area of Science:
- Metabolic and cardiovascular health
- Developmental origins of health and disease
Background:
- Reduced fetal growth is associated with metabolic and cardiovascular complications.
- These complications include cardiovascular disease, insulin resistance syndrome, dyslipidaemia, impaired glucose tolerance, and type 2 diabetes.
Purpose of the Study:
- To explore the mechanisms linking reduced fetal growth to metabolic and cardiovascular complications.
- To review hypotheses explaining the association between reduced fetal growth and insulin resistance.
Main Methods:
- Literature review of studies published in the past decade.
- Analysis of proposed hypotheses for the reduced fetal growth-insulin resistance link.
Main Results:
- Insulin resistance is a key factor in the development of these complications.
- Adipose tissue is implicated as a potential player in the underlying mechanism.
- Several hypotheses exist, including detrimental fetal environment, genetic susceptibility, or a combination.
Conclusions:
- The exact mechanism linking reduced fetal growth to insulin resistance is not fully understood.
- Genetic-environmental interactions are currently the most favored hypothesis, though not yet confirmed.
Abstract:
The metabolic and cardiovascular complications associated with reduced fetal growth have been identified in the past 10 years. These include cardiovascular disease and the insulin resistance syndrome, comprising dyslipidaemia and impaired glucose tolerance or type 2 diabetes, and they appear to result from the initial development of insulin resistance. Although the mechanism underlying the development of insulin resistance associated with reduced fetal growth remains unclear, there is some evidence that adipose tissue plays a key role. Over the past decade, several hypotheses have been proposed to explain this unexpected association. Each points to either a detrimental fetal environment, genetic susceptibility or an interaction between the two. Although yet to be confirmed, the hypothesis suggesting that the association could be the consequence of genetic-environmental interactions is at present the most attractive.
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