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Department of Surgery, Brown University School of Medicine, and the Providence Veterans Affairs Medical Center, Providence, Rhode Island 02908
In this study, we
investigated the way in which fetal insulin secretion is influenced by
interrelated changes in blood glucose and sympathoadrenal activity.
Experiments were conducted in late gestation sheep fetuses prepared
with chronic peripheral and adrenal catheters. The fetus mounted a
brisk insulin response to hyperglycemia but with only a minimal change
in the glucose-to-insulin ratio, indicating a tight coupling between
insulin secretion and plasma glucose. In well-oxygenated fetuses,
2-adrenergic blockade by idazoxan effected no change in
fetal insulin concentration, indicating the absence of a resting
sympathetic inhibitory tone for insulin secretion. With hypoxia, fetal
norepinephrine (NE) and epinephrine secretion and plasma NE increased
markedly; fetal insulin secretion decreased strikingly with the degree
of change related to extant plasma glucose concentration. Idazoxan
blocked this effect showing the hypoxic inhibition of insulin secretion
to be mediated by a specific 2-adrenergic mechanism.
2-Blockade in the presence of sympathetic activation
secondary to hypoxic stress also revealed the presence of a potent
-adrenergic stimulatory effect for insulin secretion. However, based
on an analysis of data at the completion of the study, this
-stimulatory mechanism was seen to be absent in all six fetuses that
had been subjected to a prior experimentally induced hypoxic stress but
in only one of nine fetuses not subjected to this perturbation. We
speculate that severe hypoxic stress in the fetus may, at least in the
short term, have a residual effect in suppressing the -adrenergic
stimulatory mechanism for insulin secretion.
hyperglycemia; catecholamines; idazoxan; propranolol; hypoxia
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