Effect of streptozotocin diabetes on the glycolytic flux and on fructose 2,6-bisphosphate levels in isolated rat enterocytes

• Published in: Metabolism, clinical and experimental Vol. 39; no. 8; p. 882
• Main Authors: Rossi, I, Sánchez-Arias, J A, Felíu, J E
• Format: Journal Article
• Language: English
• Published: United States 01-08-1990
• Subjects: Animals; Diabetes Mellitus, Experimental - metabolism; Epithelium - metabolism; Fructosediphosphates - metabolism; Glycolysis; Hexosediphosphates - metabolism; Intestine, Small - metabolism; Kinetics; L-Lactate Dehydrogenase - metabolism; Male; Muscle, Smooth - metabolism; Phosphofructokinase-1 - metabolism; Phosphofructokinase-2; Phosphotransferases - metabolism; Pyruvate Kinase - metabolism; Rats; Rats, Inbred Strains; Reference Values
• ISSN: 0026-0495
• DOI: 10.1016/0026-0495(90)90137-2

In epithelial cells isolated from rat small intestine and incubated in the presence of 1 mM glucose, streptozotocin-induced diabetes reduced, by 46 and 29%, respectively, the rates of both glucose utilization and L-lactate formation. These effects were accompanied by a significant decrease of enterocyte fructose 2,6-bisphosphate concentration (about 50%) and of the glycolytic flux through the reaction catalyzed by 6-phosphofructo 1-kinase. The diminution of enterocyte fructose 2,6-bisphosphate levels caused by diabetes occurred in spite of an increase of hexose 6-phosphate concentration, and was associated with a reduction in the amount of active form of 6-phosphofructo 2-kinase; total activity of this enzyme was not significantly modified. Diabetes also caused an acceleration in the rate of 3-O-methyl-D-(14C) glucose uptake and increased hexokinase activity in enterocytes. Lactate dehydrogenase, pyruvate kinase and 6-phosphofructo 1-kinase activities were not found to be significantly different in epithelial cells isolated from control or diabetic animals. Our results indicate that a reduction of the glycolytic flux in enterocytes could collaborate to increase intestinal glucose absorption in the diabetic state.