Alterations in protein metabolism and amino acid concentrations in rats fed by a high-protein (casein-enriched) diet - effect of starvation.
ABSTRACT Rats were fed with a standard laboratory diet (SLD) or a high-protein diet (HPD). After three months changes in amino acid concentration and protein metabolism were examined in fed and 24h-fasted animals. In the blood of the HPD animals sacrificed in fed state were found higher concentrations of urea, aspartate, taurine, proline, valine, isoleucine, and leucine, and lower concentrations of glycine and cysteine. The main alterations in tissues were decreased concentrations of glycine and increased concentrations of valine, isoleucine, and leucine. Differences in weight, protein concentration, protein synthesis, and proteolysis in tissues were insignificant. The exception was soleus muscle in which higher values of protein synthesis and proteolysis were found in HPD animals. The response to starvation of HPD and SLD fed animals was different. In animals fed before starvation by HPD was found more pronounced decrease in a number of individual amino acids in plasma and tissues and more pronounced decrease in protein synthesis in muscle, spleen, jejunum, and colon. It is concluded that chronic intake of HPD has not positive effect on protein balance in any tissue, results in the imbalance in aminoacidemia in extracellular and intracellular fluid, and alters the response of the organism to starvation.
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ABSTRACT: Muscle wasting is a serious complication of various clinical conditions that significantly worsens the prognosis of the illnesses. Clinically relevant models of muscle wasting are essential for understanding its pathogenesis and for selective preclinical testing of potential therapeutic agents. The data presented here indicate that muscle wasting has been well characterized in rat models of sepsis (endotoxaemia, and caecal ligation and puncture), in rat models of chronic renal failure (partial nephrectomy), in animal models of intensive care unit patients (corticosteroid treatment combined with peripheral denervation or with administration of neuromuscular blocking drugs) and in murine and rat models of cancer (tumour cell transplantation). There is a need to explore genetically engineered mouse models of cancer. The degree of protein degradation in skeletal muscle is not well characterized in animal models of liver cirrhosis, chronic heart failure and chronic obstructive pulmonary disease. The major difficulties with all models are standardization and high variation in disease progression and a lack of reflection of clinical reality in some of the models. The translation of the information obtained by using these models to clinical practice may be problematic.International Journal of Experimental Pathology 05/2012; 93(3):157-71. · 2.04 Impact Factor