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Related Experiment Videos

High glucose and insulin decrease fetal lung insulin receptor mRNA and tyrosine kinase activity in vitro

I H Gewolb1, J O'Brien, T A Palese

  • 1Division of Neonatology, University of Maryland School of Medicine, Baltimore 21201.

Biochemical and Biophysical Research Communications
|July 29, 1994
PubMed
Summary

High glucose and insulin exposure in fetal rat lungs reduces insulin receptor function and glucose uptake. This down-regulation may impair surfactant production and increase respiratory distress in infants of diabetic mothers.

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Area of Science:

  • Endocrinology
  • Developmental Biology
  • Metabolic Research

Background:

  • Insulin receptors in fetal lungs are crucial for glucose metabolism.
  • Maternal diabetes can lead to fetal hyperglycemia, impacting fetal development.
  • Respiratory distress syndrome (RDS) is a significant concern in infants of diabetic mothers.

Purpose of the Study:

  • To investigate the impact of high glucose and insulin on fetal rat lung insulin receptor function.
  • To determine the effects on insulin receptor tyrosine kinase activity, mRNA abundance, and glucose uptake.
  • To elucidate the pre-translational mechanisms of insulin receptor down-regulation.

Main Methods:

  • Fetal rat lung explants (19-22 days gestation) were cultured for 48 hours.
  • Culture conditions included low (10mM) and high (100mM) glucose, with and without added insulin.

Related Experiment Videos

  • Assessed insulin receptor tyrosine kinase activity, mRNA levels, and 3H-2-deoxy-glucose uptake.

    • Main Results:

    • Combined high glucose and insulin significantly reduced insulin receptor tyrosine kinase activity (to 77.2% of control).
    • High glucose plus insulin markedly decreased insulin receptor mRNA abundance (to 37% of control).
    • Glucose uptake was significantly reduced under high glucose + insulin conditions.

    Conclusions:

    • High glucose and insulin induce pre-translational down-regulation of fetal lung insulin receptors.
    • Impaired glucose transport and reduced insulin receptor function may affect fetal lung maturation.
    • This down-regulation could contribute to RDS in infants of poorly controlled diabetic mothers.