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Related Experiment Videos

Control of fetal insulin secretion.

B T Jackson1, G J Piasecki, H E Cohn

  • 1Department of Surgery, Brown University School of Medicine, and the Providence Veterans Affairs Medical Center, Providence, Rhode Island 02908, USA. jackson.benjamin@providence.va.gov

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|November 18, 2000
PubMed
Summary

Fetal insulin secretion is tightly linked to blood glucose. Hypoxia inhibits insulin via alpha(2)-adrenergic mechanisms, while prior stress may suppress beta-adrenergic stimulation.

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Area of Science:

  • Physiology
  • Endocrinology
  • Perinatal Medicine

Background:

  • Fetal insulin secretion is crucial for growth and development.
  • Sympathoadrenal activity plays a role in regulating fetal endocrine function.
  • Understanding fetal metabolic regulation under stress is vital for perinatal health.

Purpose of the Study:

  • To investigate the influence of blood glucose and sympathoadrenal activity on fetal insulin secretion.
  • To elucidate the adrenergic mechanisms regulating fetal insulin.
  • To assess the impact of hypoxia and prior hypoxic stress on these mechanisms.

Main Methods:

  • Chronic catheterization of late gestation sheep fetuses.
  • Infusion of alpha(2)-adrenergic antagonist (idazoxan).

Related Experiment Videos

  • Induction of hypoxia and measurement of hormonal responses (norepinephrine, epinephrine, insulin, glucose).

    • Main Results:

    • Fetal insulin secretion is tightly coupled to plasma glucose levels.
    • Hypoxia inhibits fetal insulin secretion via an alpha(2)-adrenergic mechanism.
    • A beta-adrenergic stimulatory effect on insulin secretion is observed, but suppressed after prior hypoxic stress.

    Conclusions:

    • Fetal insulin secretion is regulated by both glucose and sympathoadrenal activity.
    • Alpha(2)-adrenergic pathways mediate hypoxic inhibition of insulin secretion.
    • Prior severe hypoxic stress may lead to a persistent suppression of beta-adrenergic stimulation of fetal insulin secretion.