Effects of a leucine-enriched amino acid supplement on muscle mass, muscle strength, and physical function in post-stroke patients with sarcopenia: A randomized controlled trial.

OBJECTIVES: The aim of this study was to investigate the effects of a leucine-enriched amino acid supplement on muscle mass, muscle strength, and physical function in post-stroke patients with sarcopenia. METHODS: We conducted an eight-wk, two-parallel group intervention, randomized controlled, blinded outcome assessment among 44 post-stroke older patients with sarcopenia. Sarcopenia was defined as a loss of skeletal muscle mass and decreased muscle strength according to the Asian Working Group for Sarcopenia criteria. The intervention group (n = 21) received a leucine-enriched amino acid supplement; the control group (n = 23) did not. Both groups performed low-intensity resistance training in addition to a post-stroke rehabilitation program. A primary outcome of physical function by using the motor domain of Functional Independence Measure (FIM), and secondary outcomes of appendicular muscle mass (skeletal muscle mass index [SMI]) measured via bioelectrical impedance analysis and muscle strength as handgrip strength were measured at baseline and at the end of the intervention. RESULTS: The FIM score increased significantly in both groups over time (P < 0.01), with significantly greater improvement in the intervention group than in the control group (P < 0.045). Handgrip strength also increased significantly over time (P <0.05), with significantly greater improvement in the intervention group (P < 0.01). The SMI increased significantly in the intervention group but not in the control group over time, with significantly greater improvement in the intervention group (median estimated difference, 0.50 kg/m2; 95% confidence interval, 0.01-2.11). CONCLUSIONS: We demonstrated that an eight-wk intervention consisting of a leucine-enriched amino acid supplementation and low-intensity resistance training increased muscle mass, strength, and physical function in post-stroke patients with sarcopenia.

The skewing to Th1 induced by lentinan is directed through the distinctive cytokine production by macrophages with elevated intracellular glutathione content.

In vivo lentinan (LNT)-elicited peritoneal macrophages (Mps) showed the reduced release of prostaglandins (PGs), IL-10 and IL-6, while it endowed Mps with the elevated capability to produce IL-12 and nitric oxide (NO) upon in vitro triggering, due to the elevated intracellular glutathione (GSH) content in Mps. Deprivation of intracellular GSH completely ablated the production of IL-12. Conversely, lipopolysaccharide (LPS) induced peritoneal Mps with the reduced intracellular GSH content and the reciprocal profile of mediator production. Mps with the elevated intracelluar GSH is arbitrarily termed as reductive Mp (RMp) and that with reduced amount as oxidative Mp (OMp). OMp was converted to RMp when GSH was replenished with glutathione monoethylester (GSH-OEt). The IL-2 administration in combination with LNT exerted the synergistic induction of RMp, resulting in synergistic augmentation of IL-12, NO and reduction of IL-6 production. It was also confirmed that CD4+T cells derived of LNT-administered mice showed augmented IFN-gamma and reduced IL-4 production upon in vitro anti-CD3 stimulation. Taken together it is concluded that skewing of Th1/Th2 balance to Th1 by a beta-(1-3)-glucan, LNT, is directed through the distinctive production of IL-12 versus IL-6, IL-10 and prostaglandin E2 (PGE2) by Mps, depending on intracellular GSH redox status. To the efficient tumor immunotherapy, it may be one of the critical elements to induce a reductive form of Mps in tumor stromal tissues to maintain Th1 response.