Modulation of Blood Glucose Concentration by Vagal Nerve Stimulation

Chronic cervical vagal nerve stimulation (VNS) causes weight loss in obese patients and in experimental animal models of obesity. Furthermore, parasympathetic activity directed to the liver has been demonstrated to reduce hepatic glucose release. Thus, chronic cervical VNS may be particularly beneficial in obese type 2 diabetic patients. Here we tested the hypothesis that acute cervical VNS reduces blood glucose concentration in anesthetized rats. Sprague Dawley rats were instrumented with catheters in the left carotid artery, bipolar electrodes on the right cervical vagus nerve, and a novel telemetric glucose sensor (HD-XG, DSI) in the abdominal aorta, that allows for continuous monitoring of blood glucose concentration. Once stable mean blood pressure (106±14 mmHg), heart rate (322±25 bpm), and blood glucose concentration (157±21 mg/dL) was obtained (usually after 30-60 min) VNS (rectangular impulses, 3 V, 1 ms pulse width, 5 Hz) was initiated. The stimulator was turned on and off every 30 min for five complete on/off cycles. During the “on cycles” heart rate and mean blood pressure decreased (-79±5 bpm and -9±3 mmHg) while blood glucose concentration increased (+116±66 mg/dL). During the “off cycles” heart rate, mean blood pressure, and blood glucose concentration returned to baseline levels. A similar increase in blood glucose concentration was observed with efferent VNS after sectioning the vagus nerve cranial to the stimulation electrode. In summary, acute cervical VNS at an intensity that reduces heart rate elicits a glucogenic effect in anesthetized rats. Further studies are needed to understand the mechanisms by which acute and potentially also chronic cervical VNS may increase blood glucose.