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Pathophysiology of insulin resistance in subjects born small for gestational age

Jacques Beltrand1, Claire Lévy-Marchal

  • 1INSERM, U690, Paris, FR-75019, France; Université Paris 7, Paris, FR-75205 cedex 13, France. jacques.beltrand@inserm.fr

Best Practice & Research. Clinical Endocrinology & Metabolism
|June 10, 2008
PubMed

Insights

Reduced fetal growth is linked to long-term health issues like cardiovascular diseases and type 2 diabetes, often involving insulin resistance. Understanding fetal and early postnatal factors is key to preventing future disease risk.

Area of Science:

  • Developmental origins of health and disease
  • Metabolic and cardiovascular health
  • Perinatal and postnatal influences on long-term health

Background:

  • Reduced fetal growth is associated with increased risks of cardiovascular diseases, hypertension, dyslipidemia, and type 2 diabetes.
  • Insulin resistance is a common feature of these conditions and is implicated in their pathogenesis.
  • The precise pathways linking fetal development to later-life morbidity remain incompletely understood.

Purpose of the Study:

  • To explore the complex relationship between fetal growth, early life events, and long-term health outcomes.
  • To investigate the role of insulin resistance in mediating the effects of fetal growth on adult disease risk.
  • To consider the impact of postnatal factors in the context of fetal development for public health strategies.

Main Methods:

  • Review of existing literature on fetal growth, insulin resistance, and associated long-term health risks.
  • Analysis of proposed hypotheses including detrimental fetal environment, genetic susceptibility, and catch-up growth dynamics.
  • Consideration of epidemiological data and pathogenetic mechanisms.

Main Results:

  • Established link between reduced fetal growth and increased incidence of chronic diseases in later life.
  • Identified insulin resistance as a key factor in the development of these conditions.
  • Highlighted the interplay between fetal programming, genetic factors, and postnatal environment, particularly catch-up growth.

Conclusions:

  • The developmental origins of health and disease framework emphasizes the critical role of fetal environment in shaping long-term health trajectories.
  • Understanding the mechanisms, including insulin resistance and adiposity changes, is crucial for identifying at-risk individuals.
  • Integrating knowledge of both fetal and early postnatal influences is essential for effective public health interventions to mitigate lifelong disease risk.

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