| Autor: |
Singh D; Department of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.; Division of Gastroenterology & Liver Diseases, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA., Menghini P; Division of Gastroenterology & Liver Diseases, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.; Digestive Health Research Institute, University Hospitals Cleveland Medical Center, Cleveland, OH 44106, USA., Rodriguez-Palacios A; Division of Gastroenterology & Liver Diseases, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.; Digestive Health Research Institute, University Hospitals Cleveland Medical Center, Cleveland, OH 44106, USA.; Mouse Models Core, Silvio O'Conte Cleveland Digestive Diseases Research Core Center, Cleveland, OH 44106, USA.; Germ-Free and Gut Microbiome Core, Digestive Health Research Institute, Case Western Reserve University, Cleveland, OH 44106, USA.; Department of Molecular Biology and Microbiology, Case Western Reserve University, Cleveland, OH 44106, USA., Martino LD; Case Digestive Health Research Institute, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.; Department of Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA., Cominelli F; Division of Gastroenterology & Liver Diseases, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.; Digestive Health Research Institute, University Hospitals Cleveland Medical Center, Cleveland, OH 44106, USA.; Mouse Models Core, Silvio O'Conte Cleveland Digestive Diseases Research Core Center, Cleveland, OH 44106, USA.; Germ-Free and Gut Microbiome Core, Digestive Health Research Institute, Case Western Reserve University, Cleveland, OH 44106, USA., Basson AR; Department of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.; Division of Gastroenterology & Liver Diseases, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.; Digestive Health Research Institute, University Hospitals Cleveland Medical Center, Cleveland, OH 44106, USA. |
| Abstrakt: |
Understanding the complex link between inflammation, gut health, and dietary amino acids is becoming increasingly important in the pathophysiology of inflammatory bowel disease (IBD). This study tested the hypothesis that a leucine-rich diet could attenuate inflammation and improve gut health in a mouse model of IBD. Specifically, we investigated the effects of a leucine-rich diet on dextran sulfate sodium (DSS)-induced colitis in germ-free (GF) SAMP1/YitFC (SAMP) mice colonized with human gut microbiota (hGF-SAMP). hGF-SAMP mice were fed one of four different diets: standard mouse diet (CHOW), American diet (AD), leucine-rich AD (AD + AA), or leucine-rich CHOW diet (CH + AA). Body weight, myeloperoxidase (MPO) activity, gut permeability, colonoscopy scores, and histological analysis were measured. Mice on a leucine-rich CHOW diet showed a decrease in fecal MPO prior to DSS treatment as compared to those on a regular diet ( p > 0.05); however, after week five, prior to DSS, this effect had diminished. Following DSS treatment, there was no significant difference in gut permeability, fecal MPO activity, or body weight changes between the leucine-supplemented and control groups. These findings suggest that while a leucine-rich diet may transiently affect fecal MPO levels in hGF-SAMP mice, it does not confer protection against DSS-induced colitis symptoms or mitigate inflammation in the long term. |
