Response of glutamine metabolism to exogenous glutamine in humans.
Level 2 - randomized trial
Randomized crossover metabolic tracer study in healthy human subjects
PubMed 7485479 · doi:10.1152/ajpendo.1995.269.4.E663
What was done
A preliminary validation study in 6 healthy men compared simultaneous intravenous infusions of L-[1-13C]-, L-[U-14C]-, and L-[3,4-3H]glutamine. In the main randomized crossover trial, 5 healthy subjects in the postabsorptive state underwent two 5-hour intravenous infusions of L-[3,4-3H]glutamine paired with nasogastric L-[1-13C]glutamine infusion on separate days, randomized to receive either saline control or natural L-glutamine (856 +/- 45 µmol·kg⁻¹·h⁻¹). Plasma concentrations, splanchnic extraction, rate of appearance (Ra), oxidation, de novo synthesis, and proteolysis were measured.
What was found
Tracer-alone splanchnic extraction of glutamine was 74 +/- 4%, decreasing to 53 +/- 5% with enteral glutamine loading. Enteral glutamine significantly increased plasma glutamine (from 630 +/- 50 to 1,297 +/- 75 µM), total Ra (from 258 +/- 20 to 589 +/- 45 µmol·kg⁻¹·h⁻¹), and glutamine oxidation (from 179 +/- 20 to 477 +/- 47 µmol·kg⁻¹·h⁻¹; all P < 0.01). Endogenous de novo glutamine synthesis declined from 156 +/- 15 to 93 +/- 13 µmol·kg⁻¹·h⁻¹, whereas glutamine release from proteolysis was unchanged.
Why it matters
This study demonstrates that the splanchnic bed extracts the majority of enterally administered glutamine on first pass, and shows that acute glutamine loading suppresses endogenous de novo synthesis rather than reducing whole-body proteolysis.
Limits
The sample size was very small (n = 5), restricted to healthy adult males in an acute 5-hour postabsorptive state. Findings cannot be generalized to clinical populations (such as catabolic or critically ill patients) or long-term supplementation.
Cited by
- partial When ingested orally, the gut and liver consume the vast majority of glutamine, resulting in very little entering the bloodstream.