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1 Department of Molecular Physiology & Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA; Unite de Nutrition et Metabolisme Proteique, INRA, Centre de Recherches en Nutrition Humaine de Clermont-Fd, Ceyrat, France
2 Department of Molecular Physiology & Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA
* To whom correspondence should be addressed. E-mail: Dominique.P.Dardevet{at}vanderbilt.edu.
Whether GLP1 has insulin-independent effects on glucose disposal in vivo was assessed in conscious dogs using tracer and arteriovenous difference techniques. After a basal period, each experiment consisted of 3 periods (P1, P2, P3) during which somatostatin, glucagon, insulin and glucose were infused. The control group (C) received saline in P1,P2 and P3, the PePe group received saline in P1 and GLP1 (7.5 pmol/kg/min) peripherally (i.v) in P2 and P3 and the PePo group received saline in P1 and GLP1 peripherally (i.v) (P2) then into the portal vein (P3). Glucose and insulin concentrations increased to 2-fold and 4-fold basal, respectively and glucagon remained basal. GLP1 levels increased similarly in the PePe and PePo groups during P2 (~200pM) whereas portal GLP1 levels were significantly increased (3-fold) in PePo vs PePe during P3. In all groups, net hepatic glucose uptake (NHGU) occurred during P1. During P2, NHGU increased slightly but not significantly in all groups. During P3, NHGU increased in PePe and PePo groups to a greater extent than in C but no significant effect of the route of infusion of GLP1 was demonstrated (16.61±2.91 and 14.67±2.09 vs 4.22±1.57 µmol/kg/min, respectively). In conclusion: GLP1 increased glucose disposal in the liver independent of insulin secretion; its full action required long term infusion. The route of infusion did not modify the hepatic response.
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