Metabolism as Disease Tolerance: Implications for Sepsis-Associated Acute Kidney Injury.
Metabolism as Disease Tolerance: Implications for Sepsis-Associated Acute Kidney Injury.
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作者：
Huen SC
脓毒症是危重病人死亡的重要原因。在脓毒症中发展的代谢紊乱通常被认为是病理性的，导致败血症的发病率和死亡率。然而，脓毒症期间代谢的改变是多方面的，而且还不完全清楚。感染期间的急性厌食症是一种进化保守的反应，表明厌食症在宿主对感染的反应中具有潜在的保护作用。在细菌性炎症的动物模型中，与急性厌食症相关的禁食代谢程序，如成纤维细胞生长因子21和酮体生成，与提高存活率有关。其他禁食代谢途径，如脂肪酸氧化和自噬，也与预防急性肾脏损伤有关。脓毒症期间的全球代谢变化和当前的临床干预可能会潜在地影响疾病耐受机制，并改变急性肾损伤的风险。
Sepsis is a significant cause for mortality among critically ill patients. Metabolic derangements that develop in sepsis are often considered to be pathologic, contributing to sepsis morbidity and mortality. However, alterations in metabolism during sepsis are multifaceted and are incompletely understood. Acute anorexia during infection is an evolutionarily conserved response, suggesting a potential protective role of anorexia in the host response to infection. In animal models of bacterial inflammation, fasting metabolic programs associated with acute anorexia, such as Fibroblast Growth Factor 21 and ketogenesis, are associated with improved survival. Other fasting metabolic pathways such as fatty acid oxidation and autophagy are also implicated in preventing acute kidney injury. Global metabolic changes during sepsis and current clinical interventions can potentially affect disease tolerance mechanisms and modify the risk of acute kidney injury.
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