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 infusions of L-[1-¹³C]leucine on three separate days, while receiving intravenous infusion of 1) saline, 2) L-glutamine (800 µmol · kg¹ · h¹), and 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 order. Glutamine infusion induced a doubling in plasma glutamine level, and glycine caused a >10-fold rise in plasma glycine level. During intravenous infusions of [¹³C]leucine, the plasma leucine labeling attained a plateau value between 3.22 and 3.68 mole % excess (MPE) and [¹³C]ketoisocaproate ([¹³C]KIC) of 2.91-2.84 MPE; there were no significant differences between glutamine, glycine, and saline infusion days. Plasma leucine appearance rate was 354 ± 33 (SE), 414 ± 28, and 351 ± 35 µmol · kg¹ · h¹ (not significant) during glycine, saline, and glutamine infusion, respectively. The fractional synthetic rate (FSR) of duodenal mucosa protein was calculated from the rise in protein-bound [¹³C]leucine enrichment in the biopsy sample, divided by time and with either plasma [¹³C]KIC or tissue free [¹³C]leucine as precursor pool enrichment. Regardless of the precursor pool used in calculations, duodenal protein FSR failed to rise significantly during glutamine infusion (65 ± 11%/day) compared either with saline (84 ± 18%/day) or glycine infusion days (80 ± 15%/day). We conclude that 1) plasma [¹³C]KIC and tissue free [¹³C]leucine can be used interchangeably as precursor pools to calculate gut protein FSR; and 2) short intravenous infusion of glutamine does not acutely stimulate duodenal protein synthesis in well-nourished, growing dogs.

stable isotopes; nutrition; small intestine; [¹³C]leucine

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