Effects of Low-Protein, and Supplemented Very Low–Protein Diets, on Muscle Protein Turnover in Patients With CKD
Giacomo GaribottoAntonella SofiaE ParodiFrancesca AnsaldoAlice BonanniDaniela PicciottoAlessio SignoriMonica VettorePaolo TessariDaniela Verzola
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Abstract:
Early studies have shown that patients with chronic kidney disease (CKD) are able to maintain nitrogen balance despite significantly lower protein intake, but how and to what extent muscle protein metabolism adapts to a low-protein diet (LPD) or to a supplemented very LPD (sVLPD) is still unexplored.We studied muscle protein turnover by the forearm perfusion method associated with the kinetics of 2H-phenylalanine in patients with CKD: (i) in a parallel study in subjects randomized to usual diet (1.1 g protein/kg, n = 5) or LPD (0.55 g protein/kg, n = 6) (Protocol 1); (ii) in a crossover, self-controlled study in subjects on a 0.55 g/kg LPD followed by a sVLPD (0.45 g/kg + amino/ketoacids 0.1 g/kg, n = 6) (Protocol 2).As compared with a 1.1 g/kg containing diet, a 0.55 g/kg LPD induced the following: (i) a 17% to 40% decrease in muscle protein degradation and net protein balance, respectively, (ii) no change in muscle protein synthesis, (iii) a slight (by approximately 7%, P < 0.06) decrease in whole-body protein degradation, and (iv) an increase in the efficiency of muscle protein turnover. As compared with an LPD, an sVLPD induced the following: (i) no change in muscle protein degradation, and (ii) an approximately 50% decrease in the negative net protein balance, and an increase in the efficiency of muscle protein turnover.The results of these studies indicate that in patients with CKD the adaptation of muscle protein metabolism to restrained protein intake can be obtained via combined responses of protein degradation and the efficiency of recycling of amino acids deriving from protein breakdown.Keywords:
Protein turnover
Protein metabolism
Protein Degradation
Muscle protein
Nitrogen balance
Low-protein diet
Crossover study
The effects of growth-suppressing and muscle-wasting treatments on muscle protein turnover and amino acid concentrations were determined in vivo. All treatments depressed protein synthesis and some treatments depressed protein breakdown. Only prolonged starvation increased protein breakdown. Muscle protein mass is regulated primarily through alterations in protein synthesis in all except emergency conditions. The increased concentrations of the branched-chain amino acids indicate that they are unlikely to be involved in this regulation.
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It is well recognized that muscle makes a major contribution to amino acid and protein metabolism in the body but many of the details are still obscure. An understanding of the effects of injury and disease on muscle protein turnover and amino acid metabolism requires much more basic information on the mechanisms for the mobilization of amino acids from lean tissue and the relative contributions of different tissues. Several methodological approaches are reviewed. Our current knowledge of the effects of injury and disease on amino acid balance and protein turnover in muscle is als reviewed. It is suggested that the effects may be broadly categorized as those causing rapid increases in protein turnover with breakdown exceeding synthesis, and those in which synthesis is depressed below breakdown. The former response is more likely following severe trauma and during sepsis and the latter more common after moderate injury and during malnutrition. A knowledge of the mechanisms of loss of amino acid from muscle tissue is vital to the design of rational therapeutic intervention.
Protein turnover
Protein metabolism
Muscle protein
Catabolism
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Catabolism
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Protein turnover
Protein metabolism
Muscle protein
Protein Degradation
Myofibril
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Protein turnover
Protein metabolism
Nitrogen balance
Catabolism
Protein Degradation
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Protein metabolism
Catabolism
Protein turnover
Muscle protein
Nitrogen balance
Protein Degradation
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Protein turnover
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Low-protein diet
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Adaptation to a low-protein diet (LPD) involves a reduction in the rate of amino acid (AA) flux and oxidation, leading to more efficient use of dietary AA and reduced ureagenesis. Of note, the concept of 'adaptation' to low-protein intakes has been separated from the concept of 'accommodation', the latter term implying a decrease in protein synthesis, with development of wasting, when dietary protein intake becomes inadequate, i.e. beyond the limits of the adaptive mechanisms. Acidosis, insulin resistance and inflammation are recognized mechanisms that can increase protein degradation and can impair the ability to activate an adaptive response when an LPD is prescribed in a chronic kidney disease (CKD) patient. Current evidence shows that, in the short term, clinically stable patients with CKD Stages 3-5 can efficiently adapt their muscle protein turnover to an LPD containing 0.55-0.6 g protein/kg or a supplemented very-low-protein diet (VLPD) by decreasing muscle protein degradation and increasing the efficiency of muscle protein turnover. Recent long-term randomized clinical trials on supplemented VLPDs in patients with CKD have shown a very good safety profile, suggesting that observations shown by short-term studies on muscle protein turnover can be extrapolated to the long-term period.
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