Key result
Cervical vagal nerve stimulation impaired glucose tolerance in conscious rats, increasing the area under the blood glucose curve compared to sham stimulation (3499 vs 1810 mg/dL*h; P<0.05).
Why the study?
Because cervical VNS increases blood glucose and inhibits insulin secretion via afferent signaling in anesthetized rats, it was questioned whether VNS impairs glucose tolerance in conscious rats.
Does cervical vagal nerve stimulation impair glucose tolerance and suppress insulin release in conscious rats?
RCT (n=7)
Randomized order
Does cervical vagal nerve stimulation impair glucose tolerance and suppress insulin release in conscious rats?
Absolute Event Rate: 3499% vs 1810%
p-value: p=<0.05
Cervical vagal nerve stimulation elevates fasted blood glucose and impairs glucose tolerance in conscious rats, raising questions about potential metabolic risks in patients treated with VNS.
May warrant glucose monitoring in VNS-treated patients; leaves open effects on tolerance in conscious models.
Previously, we reported that cervical vagal nerve stimulation (VNS) increases blood glucose levels and inhibits insulin secretion in anesthetized rats through afferent signaling. Since afferent signaling is also thought to mediate the therapeutic effects of VNS in patients with therapy-refractory epilepsy and major depression, the question arises if patients treated with VNS develop impaired glucose tolerance. Thus, we hypothesized that cervical VNS impairs glucose tolerance in conscious rats. Rats (n = 7) were instrumented with telemetric blood pressure sensors and right- or left-sided cervical vagal nerve stimulators (3 V, 5 Hz, 1 msec pulse duration, 1 h on 1 h off). Glucose tolerance tests (GTTs, 1.5 g dextrose/kg BW, i.p.) were performed after overnight fasting with the stimulators on or off (sham stimulation) in randomized order separated by 3-4 days. Overnight VNS did not alter mean levels of blood pressure or heart rate, but increased fasted blood glucose levels (140 ± 13 mg/dL vs. 109 ± 8 mg/dL, P < 0.05). The area under the blood glucose concentration curves of the GTTs was larger during VNS than sham stimulation (3499 ± 211 mg/dL*h vs. 1810 ± 234 mg/dL*h, P < 0.05). One hour into the GTTs, the serum insulin concentrations had decreased during VNS (-0.57 ± 0.25 ng/mL, P < 0.05) and increased during sham stimulation (+0.71 ± 0.15 ng/mL, P < 0.05) compared to the fasted baseline levels. These results demonstrate that chronic cervical VNS elevates fasted blood glucose levels and impairs glucose tolerance likely through inhibition of glucose-induced insulin release in conscious rats. It remains to be determined if patients treated with VNS are at greater risk of developing glucose intolerance and type 2 diabetes.
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Stauss et al. (2018) reported an RCT. Cervical vagal nerve stimulation vs. Sham stimulation was evaluated on Area under the blood glucose concentration curves of the glucose tolerance tests (p=<0.05). Cervical vagal nerve stimulation impaired glucose tolerance in conscious rats, increasing the area under the blood glucose curve compared to sham stimulation (3499 vs 1810 mg/dL*h; P<0.05).
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