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1 Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, USA
2 Diabetes Research and Training Center, Vanderbilt University, Nashville, TN, USA
3 Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN, USA; Diabetes Research and Training Center, Vanderbilt University, Nashville, TN, USA
* To whom correspondence should be addressed. E-mail: stephanie.m.gustavson{at}vanderbilt.edu.
Epinephrine increases net hepatic glucose output (NHGO) mainly via increased gluconeogenesis, while glucagon increases NHGO mainly via increased glycogenolysis. The aim of the present study was to determine how the two hormones interact in controlling glucose production. In 18-h fasted conscious dogs a pancreatic clamp initially fixed insulin and glucagon at basal levels, following which one of four protocols was instituted. In G+E glucagon (1.5 ng/kg/min; portally) and epinephrine (50 ng/kg/min; peripherally) were increased, in G glucagon was increased alone, in E epinephrine was increased alone, and in C neither were increased. In G, E, and C, glucose was infused to match the hyperglycemia seen in G+E (~250 mg/dl). The areas under the curve for the increase in NHGO, after subtracting the change in C, were as follows: G=661±185, E=424±158, G+E=1178±57 mg/kg. Therefore, the overall effects of the two hormones on NHGO were additive. Additionally, glucagon exerted its full glycogenolytic effect while epinephrine exerted its full gluconeogenic effect, such that both processes increased significantly during concurrent hormone administration.
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