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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
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Instrumentation of Near-term Fetal Sheep for Multivariate Chronic Non-anesthetized Recordings
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Chronically elevated norepinephrine concentrations lower glucose uptake in fetal sheep.

Melissa A Davis1, Leticia E Camacho1, Miranda J Anderson1

  • 1School of Animal and Comparative Biomedical Sciences, University of Arizona, Tucson, Arizona.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|July 16, 2020
PubMed
Summary

Chronically high norepinephrine (NE) in fetal sheep impairs glucose uptake, indicating fetal insulin resistance. This occurs independently of nutrient or oxygen changes, highlighting NE

Keywords:
adrenergic receptorcatecholaminesinsulin secretioninsulin-stimulated glucose metabolism

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Area of Science:

  • Perinatal physiology
  • Endocrinology
  • Fetal metabolism

Background:

  • Placental insufficiency and intrauterine growth restriction (IUGR) lead to elevated fetal plasma norepinephrine (NE).
  • Understanding the direct impact of NE on fetal glucose metabolism is crucial, independent of other IUGR-related factors.

Purpose of the Study:

  • To investigate the effects of chronically elevated NE on insulin-stimulated glucose metabolism in healthy fetal sheep.
  • To determine if elevated NE causes insulin resistance in the fetus.

Main Methods:

  • Surgical catheterization of near-term fetal sheep.
  • Intravenous infusion of NE or saline (control) with controlled euglycemia.
  • Intravenous glucose tolerance tests and eu/hyperinsulinemic-euglycemic clamps to assess glucose metabolism.

Main Results:

  • NE-infused fetuses showed significantly lower rates of glucose uptake during both euinsulinemic and hyperinsulinemic clamps.
  • Insulin secretion was blunted in NE-infused fetuses during glucose tolerance tests.
  • Glucose oxidation and production were not affected by NE infusion.

Conclusions:

  • Chronic exposure to elevated NE concentrations reduces fetal glucose uptake.
  • This reduction in glucose uptake is insulin-independent, suggesting fetal insulin resistance.
  • Elevated NE directly impacts fetal glucose metabolism, separate from nutrient or oxygen availability.