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Related Experiment Videos

Nutrition, glucocorticoids and pancreas development.

B Bréant1, E Gesina, B Blondeau

  • 1INSERM Unit 690, Robert Debré Hospital, Paris, France. bernadette.breant@bhdc.jussieu.fr

Hormone Research
|April 14, 2006
PubMed
Summary

Maternal undernutrition and elevated glucocorticoids reduce fetal beta-cell mass, leading to glucose intolerance and metabolic syndrome features. Glucocorticoids are crucial for pancreatic development and beta-cell mass regulation in both normal and undernourished states.

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Area of Science:

  • Endocrinology
  • Developmental Biology
  • Metabolic Syndrome

Background:

  • Low birth weight, often caused by fetal undernutrition, is linked to adult metabolic diseases like diabetes and obesity.
  • The precise mechanisms connecting fetal undernutrition to increased disease risk remain unclear.
  • A primary defect in beta-cell development is hypothesized to underlie these long-term health consequences.

Purpose of the Study:

  • To investigate the impact of maternal undernutrition on fetal beta-cell development and its long-term metabolic consequences.
  • To elucidate the role of glucocorticoids in regulating beta-cell mass during fetal development.
  • To examine the relevance of these findings in human pancreatic development.

Main Methods:

  • A rat model of maternal undernutrition was established by reducing maternal food intake.

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  • In vitro and in vivo studies in mice, including those with genetic modifications of the glucocorticoid receptor, were performed.
  • Human embryonic pancreatic specimens were analyzed for glucocorticoid receptor and Pdx-1 expression.

    • Main Results:

    • Maternal undernutrition led to intrauterine growth retardation and a persistent decrease in beta-cell mass in rats, resulting in glucose intolerance.
    • Elevated maternal glucocorticoid concentrations were identified as a key factor reducing fetal beta-cell mass.
    • Glucocorticoid receptor signaling was found to be critical for pancreatic architecture, beta-cell survival, and expansion during development, influencing transcription factors like Pdx-1.
    • Expression of the glucocorticoid receptor and Pdx-1 in the developing human pancreas suggests a conserved role.

    Conclusions:

    • Fetal undernutrition and elevated glucocorticoids impair beta-cell development, contributing to metabolic syndrome features.
    • Glucocorticoids play a vital role in regulating beta-cell mass and pancreatic development under both normal and undernourished conditions.
    • The findings suggest a potential role for glucocorticoids in human pancreatic development, with implications for understanding metabolic disease origins.