Many investigators have begun to speculate that the sympathetic nervous system is involved in the pathophysiology of type II (noninsulin-dependent) diabetes mellitus (1–4). Recalling the early observations of Claude Bernard, who found that hyperglycemia could be produced in normal rabbits by lesioning the area of the hypothalamus, several groups have noted that hyperglycemia can be produced by chemical stimulation of the brain with morphine as well as with a variety of endogenous neuropeptides and can be abolished by bilateral adrenalectomy (1,5). Similarly, hyperglycemia has been shown to result from slow intravenous infusion of epinephrine (6) as well as from certain forms of stress that produce prolonged sympathetic discharge (7).

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