López-Lirola A, González-Reimers E, Martín Olivera R, Santolaria-Fernández F, Galindo-Martín L, Abreu-González P, González-Hernández T, Valladares-Parrilla F
Departamento de Medicina Interna, Hospital Universitario, Canary Islands, Tenerife, Spain
Food Chem Toxicol. 2003 Dec;41(12):1789-97. doi: 10.1016/s0278-6915(03)00218-7.
Protein undernutrition, alterations of hormones such as IGF-1, testosterone and cortisol, and increased lipid peroxidation-which may be related with deranged metabolism of some elements such as iron (Fe), zinc (Zn), manganese (Mn), selenium (Se) or copper (Cu)-may contribute to muscle damage in non alcoholic cirrhosis. Here, we analyse the effect of protein deficiency on muscle Cu, Fe, Zn, Mn and Se in carbon-tetrachloride (CCl(4)) induced liver cirrhosis. We also study the association between protein undernutrition and these trace elements with the activity of glutathione peroxidase (GPX), superoxide dismutase (SOD) and lipid peroxidation products, and how all these are related with muscle morphological changes in 40 male adult Sprague-Dawley rats. Liver cirrhosis was induced by intraperitoneal injection of CCl(4) to 10 rats fed a 2% protein diet, and to another 10 fed a 18% protein control diet. Two further groups included rats without cirrhosis fed the 2% protein and the 18% protein diets. After sacrifice (6 weeks later), we found type IIa fibre atrophy in the cirrhotic animals, especially in the low-protein fed ones and this was due to protein deficiency. Muscle Fe increased in low protein fed cirrhotic rats. No relationship was found between muscle changes and any of the hormones, enzymes and trace elements analysed, or with liver fibrosis. These results suggest that muscle atrophy observed in CCl(4)-induced cirrhosis is related with protein deficiency, but not with cirrhosis itself.
蛋白质营养不良、胰岛素样生长因子-1(IGF-1)、睾酮和皮质醇等激素的改变以及脂质过氧化增加(这可能与铁(Fe)、锌(Zn)、锰(Mn)、硒(Se)或铜(Cu)等某些元素的代谢紊乱有关)可能导致非酒精性肝硬化中的肌肉损伤。在此,我们分析了蛋白质缺乏对四氯化碳(CCl₄)诱导的肝硬化大鼠肌肉中铜、铁、锌、锰和硒的影响。我们还研究了蛋白质营养不良与这些微量元素与谷胱甘肽过氧化物酶(GPX)、超氧化物歧化酶(SOD)活性及脂质过氧化产物之间的关联,以及所有这些如何与40只成年雄性Sprague-Dawley大鼠的肌肉形态变化相关。通过向10只喂食2%蛋白质饮食的大鼠和另外10只喂食18%蛋白质对照饮食的大鼠腹腔注射CCl₄诱导肝硬化。另外两组包括未患肝硬化但分别喂食2%蛋白质和18%蛋白质饮食的大鼠。在处死(6周后)后,我们发现肝硬化动物中IIa型纤维萎缩,尤其是低蛋白饮食组,这是由于蛋白质缺乏所致。低蛋白饮食的肝硬化大鼠肌肉中铁含量增加。未发现肌肉变化与所分析的任何激素、酶和微量元素之间存在关联,也未发现与肝纤维化有关。这些结果表明,在CCl₄诱导的肝硬化中观察到的肌肉萎缩与蛋白质缺乏有关,而与肝硬化本身无关。