OXIDATION OF GLUCOSE CARBON ENTERING THE TCA CYCLE IS REDUCED BY GLUTAMINE IN SMALL-INTESTINE EPITHELIAL-CELLS

The influence of glutamine on glucose oxidation was assessed in epithe lial cells isolated from the mucosa of the proximal, mid-, and distal small intestine of young, fed, male rats. Glucose oxidation declined a long the length of the small intestine, with values from the mid- and distal segments representing similar to 55% and 40%, respectively, of the value from the proximal segment. A gradient along the small intest ine was noted also in the influence of glutamine on glucose oxidation: glutamine suppressed glucose oxidation similar to 60% in the proximal small intestine, 39% in the mid-intestine, and 31% in the distal smal l intestine. Glutamine suppressed the oxidation of glucose carbon that entered the tricarboxylic acid (TCA) cycle; this was determined using CO2 ratios derived from acetate and glucose isotopes. In cells from t he proximal segment, the probability that carbon entering the cycle wo uld complete one full turn was reduced by glutamine from 0.77 to 0.28. The entry of glucose-derived pyruvate into the TCA cycle did not appe ar to be influenced by the presence of glutamine, however. Glutamine h ad no influence on the proportion of glucose metabolism that occurred via the pentose phosphate pathway (which averaged 5% or less), but red uced flux of carbon through pyruvate carboxylase relative to flux thro ugh pyruvate dehydrogenase from 40% to 9% in cells from the proximal s egment. These data suggest that, in the presence of glutamine, the fat e of pyruvate carbon (derived from glucose or elsewhere) entering the TCA cycle is altered from that of oxidation to anaplerosis and subsequ ent efflux of TCA cycle intermediates into newly synthesized compounds .