The route of nutrient delivery affects insulin sensitivity and liver glucose transporter expression in rat. Colomb, Virginie, Armelle Leturque, Gw[acute]ena[diaeresis]ele Guihot, Martine Loizeau, S[acute]ebastien Lavie, Sophie Colomer, Claude Ricour, Jean Girard. Centre de Recherche sur l'Endocrinologie Mol[acute]eculaire et le D[acute]eveloppement, CNRS, 9 rue Jules Hetzel, 92190 Meudon -Bellevue, France, Service de gastroent[acute]erologie et nutrition p[acute]ediatriques, H[circumflex]opital Necker-Enfants Malades, 149 rue de S[grave]evres, 75743 Paris C[acute]edex 15 and Laboratoire de chirurgie exp[acute]erimentale (section nutrition) Facult[acute]e Necker-Enfants Malades, 156 rue de Vaugirard, 75730 Paris C[acute]edex 15, France
APStracts 2:0121E, 1995.
In order to optimize artificial nutrition (AN) techniques for patients suffering from malnutrition or reduced intestinal absorption, utilization of energy fuels, especially glucose, requires better understanding. Since the liver plays a key role in glucose homeostasis, the aim of this study was to assess the effects of continuous intragastric (IG) and intravenous (IV) nutrition on insulin secretion and several markers of liver glucose metabolism, especially glucose transporter GLUT2. Wistar male rats underwent catheterization of either stomach (IG) or vena cava (IV) and received 24 h/day the same all-in-one formula over 7 or 14 days. The metabolic parameters from IG-fed rats did not differ significantly from those from orally fed control rats. IV nutrition induced insulin resistance (marked hyperinsulinemia /mild hyperglycemia) and reduced liver GLUT2 protein and mRNA levels. The decrease in liver GLUT2 gene expression might be mediated either by an inhibitory role of hyperinsulinemia or by the decrease in gut or portal factors. These results suggest that the route of nutrient delivery influences their utilization by the liver. 

Received 2 March 1995; accepted in final form 18 May 1995.
APS Manuscript Number E702-5.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 May 1995.