Effect of intravenous glutamine on duodenal mucosa protein synthesis in healthy growing dogs

To determine whether glutamine acutely stimulates protein synthesis in the duodenal mucosa, five healthy growing dogs underwent endoscopic biopsies of duodenal mucosa at the end of three 4-h primed, continuous intravenous inf usions of L-[1-C-13]leucine on three separate days, while receiving intrave nous infusion of 1) saline, 2) L-glutamine (800 mu mol . kg(-1) . h(-1)), a nd 3) isonitrogenous amounts of glycine. The three infusions were performed after 24 h of fasting, a week apart from each other and in a randomized or der. Glutamine infusion induced a doubling in plasma glutamine level, and g lycine caused a >10-fold rise in plasma glycine level. During intravenous i nfusions of [C-13]leucine, the plasma leucine labeling attained a plateau v alue between 3.22 and 3.68 mole % excess (MPE) and [C-13]ketoisocaproate ([ C-13]KIC) of 2.91-2.84 MPE; there were no significant differences between g lutamine, glycine, and saline infusion days. Plasma leucine appearance rate was 354 +/- 33 (SE), 414 +/- 28, and 351 + 35 mu mol . kg(-1) . h(-1) (not significant) during glycine, saline, and glutamine infusion, respectively. The fractional synthetic rate (FSR) of duodenal mucosa protein was calcula ted from the rise in protein-bound [C-13]leucine enrichment in the biopsy s ample, divided by time and with either plasma [C-13]KIC or tissue free [C-1 3]leucine as precursor pool enrichment. Regardless of the precursor pool us ed in calculations, duodenal protein FSR failed to rise significantly durin g glutamine infusion (65 +/- 11%/day) compared either with saline (84 +/- 1 8%/day) or glycine infusion days (80 +/- 15%/ day). We conclude that 1) pla sma [C-13]KIC and tissue free [C-13]leucine can be used interchangeably as precursor pools to calculate gut protein FSR; and 2) short intravenous infu sion of glutamine does not acutely stimulate duodenal protein synthesis in well-nourished, growing dogs.