Horm Metab Res 1989; 21(12): 643-645
DOI: 10.1055/s-2007-1009309
Originals Basic

© Georg Thieme Verlag, Stuttgart · New York

Involvement of Adrenergic Mechanism in Hyperglycemia Due to SCN Stimulation

T. Fujii1 , S. Inoue1 , K. Nagai2 , H. Nakagawa2
  • 1Third Department of Internal Medicine, Yokohama City University, Yokohama
  • 2Division of Protein Metabolism, Institute for Protein Research, Osaka University, Suita, Osaka, Japan
Further Information

Publication History

1989

1989

Publication Date:
14 March 2008 (online)

Summary

Previously we found that in rats, electrical stimulation of the suprachiasmatic nucleus (SCN) of the hypothalamus elicited hyperglycemia associated with hyperglucagonemia without immediate hyperinsulinemia. To clarify the mechanism of these responses, we examined the effects of blockers of the autonomic nervous system on these responses. Hexamethonium, a ganglion blocker, suppressed the hyperglycemic and hyperglucagonemic responses to electrical stimulation of the SCN. Both bunazosin, an α1-adrenergic blocker, and yohimbin, an α2-adrenergic blocker, increased the level of insulin before stimulation, but only the latter suppressed the hyperglycemic and hyperglucagonemic responses. Propranolol, a β-adrenergic blocker, partially inhibited the responses. These findings suggest that α2- and β-adrenergic mechanisms are involved in the hyperglycemic and hyperglucagonemic responses to SCN stimulation.

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