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Published on: November 20, 2015
Long-term metabolic consequences of being born small for gestational age
Claire Levy-Marchal1, Delphine Jaquet, Paul Czernichow
1INSERM Unit 457, Robert Debré Hospital, 75019 Paris, France. clairelm@inserm.fr
Insights
Fetal growth restriction may lead to type 2 diabetes and obesity later in life. Catch-up growth and early postnatal development are critical factors in metabolic health.
Area of Science:
- Endocrinology
- Metabolic disease research
- Developmental biology
Background:
- Fetal growth restriction is linked to long-term metabolic disorders.
- Adipose tissue plays a key role in metabolic complications after restricted fetal growth.
- The precise mechanisms linking fetal growth restriction to insulin resistance are not fully understood.
Purpose of the Study:
- To review evidence on the fetal and early origins of type 2 diabetes, insulin resistance, dyslipidaemia, and obesity.
- To emphasize the role of adipose tissue in catch-up growth and metabolic outcomes following fetal growth restriction.
Main Methods:
- Literature review of existing evidence.
- Analysis of proposed pathways for insulin resistance development.
- Focus on the impact of adipose tissue and growth patterns.
Main Results:
- Evidence suggests a connection between fetal growth restriction and later metabolic diseases.
- Adipose tissue's role in catch-up growth is implicated in metabolic complications.
- Several potential pathways for insulin resistance have been proposed but not definitively proven.
Conclusions:
- Fetal and early life growth significantly influence the risk of developing type 2 diabetes, insulin resistance, dyslipidaemia, and obesity.
- Early postnatal growth is also a critical period for metabolic health.
- Further research is needed to elucidate the precise mechanisms involved.
Abstract:
This article reviews the evidence for fetal and early origins of type 2 diabetes, insulin resistance, dyslipidaemia and obesity. Particular emphasis is given to the role of adipose tissue in catch-up growth and long-term metabolic complications following restricted fetal growth. To date, several pathways have been proposed to explain the development of insulin resistance following restricted fetal growth, but no precise mechanisms have been demonstrated. It appears that early postnatal growth may also be a critical step.
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