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Glutamine Supplementation Increases Postprandial Energy Expenditure and Fat Oxidation in Humans

From the Center for Designing Foods to Improve Nutrition, Department of Food Science and Human Nutrition, Iowa State University, Ames, Iowa

Correspondence: Shawn Baier, MS, Food Science and Human Nutrition, Iowa State University, Ames, IA 50011. Electronic mail may be sent to baier{at}iastate.edu.

Background: Glutamine interacts with insulin-mediated glucose disposal, which is a component of the increase in energy expenditure (EE) after a meal. The study aim was to examine if glutamine supplementation alters postmeal nutrient oxidation. Methods: Ten healthy young adults consumed a mixed meal (6.5 kcal/kg, 14%:22%:64% = protein:fat:carbohydrate) containing either glutamine (GLN:1.05 kcal/kg) or an isocaloric amino acid mixture (alanine: glycine:serine = 2:1:0.5; CON). GLN and CON treatments were administered on separate days in random order for each subject. EE, nonprotein respiratory quotient (RQ), and fat and carbohydrate oxidation rates were assessed using indirect calorimetry for 30 minutes before and for 360 minutes after meal ingestion. Results: Premeal EE and RQ were similar between treatments. The increase in EE above basal during both early (0–180 minutes) and late (180–360 minutes) postmeal phases was greater in GLN than in CON (p < .05), resulting in postmeal EE being 49% greater during the total postmeal phase (p < .05). Net change of carbohydrate oxidation was 38% higher during the early phase with GLN (p < .05), whereas it was 71% lower during the later phase (p < .05). GLN enhanced fat oxidation by 42 kcal compared with CON during the late phase (p < .05). Conclusions: Glutamine supplementation with a mixed meal alters nutrient metabolism to increase postmeal EE by increasing carbohydrate oxidation during the early postmeal phase and fat oxidation during the late postmeal phase. Consideration must be given to the potential that these postprandial changes in EE are related to glutamine-mediated changes in insulin action and consequently glucose disposal.

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