ABSTRACT
This study investigated the effects of l-glutamine (Gln) and/or l-leucine (Leu) administration on sepsis-induced skeletal muscle injuries. C57BL/6J mice were subjected to cecal ligation and puncture to induce polymicrobial sepsis and then given an intraperitoneal injection of Gln, Leu, or Gln plus Leu beginning at 1 h after the operation with re-injections every 24 h. All mice were sacrificed on either day 1 or day 4 after the operation. Blood and muscles were collected for analysis of inflammation and oxidative damage-related biomolecules. Results indicated that both Gln and Leu supplementation alleviated sepsis-induced skeletal muscle damage by reducing monocyte infiltration, calpain activity, and mRNA expression levels of inflammatory cytokines and hypoxia-inducible factor-1α. Furthermore, septic mice treated with Gln had higher percentages of blood anti-inflammatory monocytes and muscle M2 macrophages, whereas Leu treatment enhanced the muscle expressions of mitochondrion-related genes. However, there were no synergistic effects when Gln and Leu were simultaneously administered. These findings suggest that both Gln and Leu had prominent abilities to attenuate inflammation and degradation of skeletal muscles in the early and/or late phases of sepsis. Moreover, Gln promoted the switch of leukocytes toward an anti-inflammatory phenotype, while Leu treatment maintained muscle bioenergetic function.
Subject(s)
Anti-Inflammatory Agents/therapeutic use , Glutamine/therapeutic use , Leucine/therapeutic use , Muscle, Skeletal/injuries , Sepsis/pathology , Animals , Calpain/metabolism , Cytokines/biosynthesis , Hypoxia-Inducible Factor 1, alpha Subunit/biosynthesis , Inflammation/prevention & control , Macrophages/physiology , Male , Mice , Mice, Inbred C57BL , Monocytes/physiology , Muscle, Skeletal/pathology , Oxidative Stress/drug effectsABSTRACT
BACKGROUND: Postoperative weight loss and malnutrition are major issues in gastric cancer patients. The concept of oral nutritional supplements (ONS) is gaining widespread acceptance. We investigated the effects of ONS administration on postoperative body weight loss in patients with gastric cancer who had undergone total gastrectomy or distal gastrectomy. METHODS: Patients were randomized to either the treatment or the control group. In both groups, standard surgery for gastric cancer was performed. In the treatment group, intervention with ONS was performed until 12 weeks after discharge. In the control group, patients were fed the usual postoperative diet. Weight, body composition, quality of life, hematological parameters, and blood chemistry were evaluated. RESULTS: We analyzed 113 cases (73 distal gastrectomy, 40 total gastrectomy). Weight loss in the ONS group after total gastrectomy was significantly less than that in the control group. Weight loss and skeletal muscle mass loss after distal gastrectomy did not differ significantly between the ONS and control groups. CONCLUSION: This study showed ONS after total gastrectomy to significantly diminish postoperative weight loss.
Subject(s)
Dietary Supplements , Gastrectomy , Postoperative Care , Stomach Neoplasms/surgery , Weight Loss , Administration, Oral , Adult , Aged , Body Composition , Female , Humans , Male , Middle Aged , Quality of LifeABSTRACT
BACKGROUND: Migration of T cells into the colon plays a major role in the pathogenesis in inflammatory bowel disease. This study investigated the effects of glutamine (Gln) supplementation on chemokine receptors and adhesion molecules expressed by T cells in mice with dextran sulfate sodium- (DSS-) induced colitis. METHODS: C57BL/6 mice were fed either a standard diet or a Gln diet replacing 25% of the total nitrogen. After being fed the diets for 5 days, half of the mice from both groups were given 1.5% DSS in drinking water to induce colitis. Mice were killed after 5 days of DSS exposure. RESULTS: DSS colitis resulted in higher expression levels of P-selectin glycoprotein ligand- (PSGL-) 1, leukocyte function-associated antigen- (LFA-) 1, and C-C chemokine receptor type 9 (CCR9) by T helper (Th) and cytotoxic T (Tc) cells, and mRNA levels of endothelial adhesion molecules in colons were upregulated. Gln supplementation decreased expressions of PSGL-1, LFA-1, and CCR9 by Th cells. Colonic gene expressions of endothelial adhesion molecules were also lower in Gln-colitis mice. Histological finding showed that colon infiltrating Th cells were less in the DSS group with Gln administration. CONCLUSIONS: Gln supplementation may ameliorate the inflammation of colitis possibly via suppression of T cell migration.