PURPOSE: Vagal interruption causes weight loss in humans and decreases endogenous glucose production in animals. However, it is unknown if this is due to a direct effect on glucose metabolism. We sought to determine if vagal blockade using electrical impulses alters glucose metabolism in humans. PATIENTS AND METHODS: We utilized a randomized, cross-over study design where participants were studied after 2 weeks of activation or inactivation of vagal nerve blockade (VNB). Seven obese subjects with impaired fasting glucose previously enrolled in a long-term study to examine the effect of VNB on weight took part. We used a standardized triple-tracer mixed meal to enable measurement of the rate of meal appearance, endogenous glucose production, and glucose disappearance. The 550 kcal meal was also labeled with (111)In-diethylene triamine pentaacetic acid (DTPA) to measure gastrointestinal transit. Insulin action and beta-cell responsivity indices were estimated using the minimal model. RESULTS: Integrated glucose, insulin, and glucagon concentrations did not differ between study days. This was also reflected in a lack of effect on beta-cell responsivity and insulin action. Furthermore, fasting and postprandial endogenous glucose production, integrated meal appearance, and glucose disposal did not differ in the presence or absence of VNB. Similarly, gastric emptying and colonic transit were unchanged by VNB. CONCLUSION: In this pilot study in nondiabetic humans, electrical vagal blockade had no acute effects on glucose metabolism, insulin secretion and action, or gastric emptying. It remains to be determined if more pronounced effects would be observed in diabetic subjects.

The effect of vagal nerve blockade using electrical impulses on glucose metabolism in nondiabetic subjects

PICCININI, FRANCESCA;DALLA MAN, CHIARA;COBELLI, CLAUDIO;
2014

Abstract

PURPOSE: Vagal interruption causes weight loss in humans and decreases endogenous glucose production in animals. However, it is unknown if this is due to a direct effect on glucose metabolism. We sought to determine if vagal blockade using electrical impulses alters glucose metabolism in humans. PATIENTS AND METHODS: We utilized a randomized, cross-over study design where participants were studied after 2 weeks of activation or inactivation of vagal nerve blockade (VNB). Seven obese subjects with impaired fasting glucose previously enrolled in a long-term study to examine the effect of VNB on weight took part. We used a standardized triple-tracer mixed meal to enable measurement of the rate of meal appearance, endogenous glucose production, and glucose disappearance. The 550 kcal meal was also labeled with (111)In-diethylene triamine pentaacetic acid (DTPA) to measure gastrointestinal transit. Insulin action and beta-cell responsivity indices were estimated using the minimal model. RESULTS: Integrated glucose, insulin, and glucagon concentrations did not differ between study days. This was also reflected in a lack of effect on beta-cell responsivity and insulin action. Furthermore, fasting and postprandial endogenous glucose production, integrated meal appearance, and glucose disposal did not differ in the presence or absence of VNB. Similarly, gastric emptying and colonic transit were unchanged by VNB. CONCLUSION: In this pilot study in nondiabetic humans, electrical vagal blockade had no acute effects on glucose metabolism, insulin secretion and action, or gastric emptying. It remains to be determined if more pronounced effects would be observed in diabetic subjects.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11577/3156062
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