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This version published online on August 7, 2007
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2007-0536
A more recent version of this article appeared on October 1, 2007
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Right arrow Diabetes and Insulin

Submitted on March 9, 2007
Accepted on July 26, 2007

Tyramine-Mediated Activation of Sympathetic Nerves Inhibits Insulin Secretion in Humans

Lisa K. Gilliam*, Jerry P. Palmer, and Gerald J. Taborsky Jr

Department of Medicine, University of Washington and Veterans Affairs Puget Sound Health Care System

* To whom correspondence should be addressed. E-mail: lgilliam{at}u.washington.edu.

Context: Older studies have shown that high doses of norepinephrine infused into human subjects can inhibit insulin secretion. Similar inhibition during electrical stimulation of sympathetic nerves in animals raises the possibility that the suppression of insulin secretion seen in humans could reflect a physiologic effect of sympathetic nerves on islet beta-cells. However, a direct test of the hypothesis that moderate and selective activation of these nerves is sufficient to inhibit insulin secretion in humans is lacking.

Objective: We sought to test this hypothesis by releasing moderate amounts of endogenous NE selectively from the sympathetic nerves of normal human subjects by infusing them with low doses of the indirect sympathomimetic agent, tyramine.

Methods: During a single study visit, eleven healthy subjects received intravenous injections of arginine either alone, or in combination with a low dose tyramine infusion. Physiological (blood pressure) and biochemical (insulin, glucose, norepinephrine) parameters were measured.

Results: The acute insulin response to arginine was significantly reduced during tyramine, compared to that seen in the absence of tyramine (p=0.036).

Conclusions: These data suggest that moderate and selective activation of sympathetic nerves inhibits insulin release in humans.


Key words: tyramine • sympathetic nerves • insulin secretion • pancreas







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