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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
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.
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).
- 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.