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Am J Physiol Endocrinol Metab 283: E958-E964, 2002; doi:10.1152/ajpendo.00566.2001
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Vol. 283, Issue 5, E958-E964, November 2002

Involvement of the vagus nerves in the regulation of basal hepatic glucose production in conscious dogs

Sylvain Cardin1,2, Konstantin Walmsley3, Doss W. Neal3, Phillip E. Williams3, and Alan D. Cherrington1,3

1 Department of Molecular Physiology and Biophysics, 3 Diabetes Research and Training Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0615; and 2 Department of Neuroscience, Pro-Neuron, Gaithersburg, Maryland 20877

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°C solution, while in the other (Cool, n = 6), the coils were perfused with -20°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.

vagal cooling; liver nerves; parasympathetic blockade; gluconeogenesis; glycogenolysis


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