Mitch W E
Renal Division, Emory University School of Medicine, Atlanta, GA 30322, USA.
Miner Electrolyte Metab. 1996;22(1-3):62-5.
It is well established that chronic renal failure is associated with loss of lean body mass. Possible explanations for protein losses include a limited ability to reduce essential amino acid oxidation and protein degradation when dietary protein is low. Alternatively, uremia could directly stimulate protein catabolism. In rats, we have uncovered evidence that metabolic acidosis not only blunts the responses to a low-protein diet but also stimulates the degradation of muscle protein. We find that the ATP-ubiquitin-proteasome-dependent pathway causing muscle protein degradation is activated by acidosis. Glucocorticoids are required but are not sufficient to elicit this catabolic response.
众所周知，慢性肾衰竭与瘦体重的丧失有关。蛋白质损失的可能解释包括当饮食蛋白质含量低时，减少必需氨基酸氧化和蛋白质降解的能力有限。另外，尿毒症可能直接刺激蛋白质分解代谢。在大鼠中，我们发现有证据表明，代谢性酸中毒不仅会减弱对低蛋白饮食的反应，还会刺激肌肉蛋白的降解。我们发现，导致肌肉蛋白降解的ATP-泛素-蛋白酶体依赖性途径被酸中毒激活。糖皮质激素是必需的，但不足以引发这种分解代谢反应。
