• Éder Ricardo Petry, Diego de Freitas Dresch, Clarice Carvalho, Patricia Calçada Medeiros, Tatiana Gomes Rosa, Cleverson Morais de Oliveira, Leo Anderson Meira Martins, Fátima Costa Rodrigues Guma, Norma Possas Marroni, and Clóvis Milton Duval Wannmacher.
• Department of Cellular and Molecular Physiology, College of Medicine, Penn State University, Hershey, Pennsylvania, USA; Post-Graduate Program in Biological Sciences: Biochemistry, Institute of Basic Health Sciences (ICBS), Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, Rio Grande do Sul, Brazil; Department of Biochemistry, ICBS, UFRGS, Porto Alegre, Rio Grande do Sul, Brazil. Electronic address: eder.petry44@gmail.com.
• Nutrition. 2024 Feb 1; 118: 112273112273.

BackgroundSkeletal muscle synthesizes, stores, and releases body L-glutamine (GLN). Muscle atrophy due to disabling diseases triggers the activation of proteolytic and pro-apoptotic cell signaling, thus impairing the body's capacity to manage GLN content. This situation has a poor therapeutic prognosis.ObjectiveEvaluating if oral GLN supplementation can attenuate muscle wasting mediated by elevated plasma cortisol and activation of caspase-3, p38MAPK, and FOXO3a signaling pathways in soleus and gastrocnemius muscles of rats submitted to 14-day bilateral hindlimbs immobilization.MethodsAnimals were randomly distributed into six groups: non-immobilized rats (Control), control orally supplemented with GLN (1 g kg-1) in solution with L-alanine (ALA: 0.61 g kg-1; GLN+ALA), control orally supplemented with dipeptide L-alanyl-L-glutamine (DIP; 1.49 g kg-1), hindlimbs immobilized rats (IMOB), IMOB orally GLN+ALA supplemented (GLN+ALA-IMOB), and IMOB orally DIP supplemented (DIP-IMOB). Plasma and muscle GLN concentration, plasma cortisol level, muscle caspase-3 activity, muscle p38MAPK and FOXO3a protein content (total and phosphorylated forms), and muscle cross-sectional area (CSA) were measured.ResultsCompared to controls, IMOB rats presented: a) increased plasma cortisol levels; b) decreased plasma and muscle GLN concentration; c) increased muscle caspase-3 activity; d) increased total and phosphorylated p38MAPK protein content; e) increased FOXO3a and decreased phosphorylated FOXO3a protein content; f) reduced muscle weight and CSA befitting to atrophy. Oral supplementation with GLN+ALA and DIP was able to significantly attenuate these effects.ConclusionsThese findings attest that oral GLN supplementation in GLN+ALA solution or DIP forms attenuates rats' skeletal muscle mass wasting caused by disuse-mediated muscle atrophy.Copyright © 2023 Elsevier Inc. All rights reserved.

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