AJP - Endocrinology and Metabolism, Vol 254, Issue 4 E468-E475, Copyright © 1988 by American Physiological Society
Hyperglycemia induced by electrical stimulation of lateral part of dorsal parabrachial nucleus
T. Fujiwara, K. Nagai, S. Takagi and H. Nakagawa
Division of Protein Metabolism, Osaka University.
Electrical stimulation of the lateral part of the dorsal parabrachial
nucleus (PBD) induces hyperglycemia by enhancing glucagon secretion and
suppressing insulin secretion in rats. The mechanism of this effect in the
light period was examined by use of blockers of the autonomic nervous
system. Hexamethonium, a ganglion blocker, and propranolol, a
beta-adrenergic blocker, markedly inhibited the hyperglycemic response to
stimulation of the lateral part of the PBD (LPBD). In contrast,
phenoxybenzamine, an alpha-adrenergic blocker, and atropine methylnitrate,
a muscarinic blocker, had no effect. Because previous studies showed that
bilateral lesions of the suprachiasmatic nucleus (SCN) eliminated
hyperglycemia induced by intracranial injection of 2-deoxy-D-glucose and
that blinding largely suppressed the hyperglycemia, the effects of these
two treatments on hyperglycemia induced by electrical stimulation of the
LPBD were examined. SCN lesions abolished the hyperglycemic response but
did not affect the hyperglucagonemic response. Results 4 wk after orbital
enucleation were similar to those after SCN lesions. These findings suggest
that the SCN and a beta-adrenergic mechanism are involved in the
hyperglycemic response to LPBD stimulation.
