Cardin Sylvain, Walmsley Konstantin, Neal Doss W, Williams Phillip E, Cherrington Alan D
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0615, USA.
Am J Physiol Endocrinol Metab. 2002 Nov;283(5):E958-64. doi: 10.1152/ajpendo.00566.2001.
We determined if blocking transmission in the fibers of the vagus nerves would affect basal hepatic glucose metabolism in the 18-h-fasted conscious dog. A pancreatic clamp (somatostatin, basal portal insulin, and glucagon) was employed. A 40-min control period was followed by a 90-min test period. In one group, stainless steel cooling coils (Sham, n = 5) were perfused with a 37 degrees C solution, while in the other (Cool, n = 6), the coils were perfused with -20 degrees C solution. Vagal blockade was verified by heart rate change (80 +/- 9 to 84 +/- 14 beats/min in Sham; 98 +/- 12 to 193 +/- 22 beats/min in Cool). The arterial glucose level was kept euglycemic by glucose infusion. No change in tracer-determined glucose production occurred in Sham, whereas in Cool it dropped significantly (2.4 +/- 0.4 to 1.9 +/- 0.4 mg. kg(-1). min(-1)). Net hepatic glucose output did not change in Sham but decreased from 1.9 +/- 0.3 to 1.3 +/- 0.3 mg. kg(-1). min(-1) in the Cool group. Hepatic gluconeogenesis did not change in either group. These data suggest that vagal blockade acutely modulates hepatic glucose production by inhibiting glycogenolysis.
我们研究了阻断迷走神经纤维的传导是否会影响禁食18小时的清醒犬的基础肝脏葡萄糖代谢。采用了胰腺钳夹(生长抑素、基础门静脉胰岛素和胰高血糖素)。先有40分钟的对照期,随后是90分钟的测试期。一组(假手术组,n = 5)用37℃溶液灌注不锈钢冷却线圈,而另一组(冷却组,n = 6)用-20℃溶液灌注。通过心率变化验证迷走神经阻断情况(假手术组心率从80±9次/分钟变为84±14次/分钟;冷却组从98±12次/分钟变为193±22次/分钟)。通过输注葡萄糖使动脉血糖水平维持在正常血糖范围。假手术组中,示踪剂测定的葡萄糖生成无变化,而冷却组中其显著下降(从2.4±0.4降至1.9±0.4毫克·千克⁻¹·分钟⁻¹)。假手术组的肝脏葡萄糖净输出无变化,但冷却组从1.9±0.3降至1.3±0.3毫克·千克⁻¹·分钟⁻¹。两组的肝脏糖异生均无变化。这些数据表明,迷走神经阻断通过抑制糖原分解急性调节肝脏葡萄糖生成。