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Laboratoire Physiopathologie Nutrition, CNRS ESA 7059, Université Paris, P7/D. Diderot, 75251 Paris Cedex 05, France
Address all correspondence and requests for reprints to: Prof. B. Portha, Laboratoire Physiopathology of Nutrition, CNRS ESA 7059, Université Paris, 7/D. Diderot, 2 place Jussieu, Tour 33, 75251 Paris Cedex 05, France. E-mail: portha{at}paris7.jussieu.fr
Glucose-induced insulin secretion in vivo is known to be
severely blunted in the rat as a consequence of protein-energy
restriction starting early in life. We have recently reported in such
malnourished rats (M rats) that the release of the counterregulatory
hormones that defend against hypoglycemia was severely disturbed, and
their plasma levels of epinephrine and norepinephrine were prominently
increased. Knowing that the autonomic nervous system has the potential
to play a major role in the control of insulin secretion in response to
glucose in vivo, we therefore determined whether
protein-energy restriction starting after weaning could alter
sympathetic and/or parasympathetic nerve activities, and whether these
changes could be responsible for the lack of response to glucose of
their ß-cells in vivo. When tested in the basal
postabsorptive state, the malnourished rats exhibited profound
alterations of both parasympathetic and sympathetic nerve activities;
the firing rates of the vagus nerve and the superior cervical ganglion
were dramatically decreased and increased, respectively. Under the same
conditions, insulin secretion in vivo in response to a
glucose load (
I/G) was severely decreased in M rats compared with
that in control (C) rats. When evaluated after administration of
acetylcholine, I was amplified to the same extent in M rats as in C
rats. After administration of the 
2A-adrenergic agonist
oxymetazoline, glucose-induced insulin release in M rats was not
significantly affected, whereas it was sharply decreased in C rats.
Finally, administration of yohimbine, an 2-adrenergic
antagonist, partially restored the lack of reactivity of the ß-cells
to glucose in the M rats, as I/G was amplified by 6-fold in the M
group and by 3.3-fold in the C group. We conclude that protein-energy
restriction starting early in life in rats brings about changes in the
overall activity of the autonomic nervous system that, in turn, are
responsible at least in part for the acquisition/maintenance of
decreased ß-cell reactivity to glucose in vivo.
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