以下文章来源于肥胖世界ObesityWorld ，作者欢迎订阅 肥胖世界ObesityWorld . 《肥胖世界》Obesity World - 同步传真肥胖及代谢国际新学术进展，为医学减重临床、教研人员搭建一座与国际接轨的桥梁，「每医健」旗下内容平台。 虽然身体成分常被误解为被动的脆弱指标，实际上它们积极参与整体代谢调节，在应对急性损伤后的生存中起到关键作用。危重症时，肌肉 与脂肪组织会发生显著调整，这不仅影响住院期间，还会深刻改变出院后的代谢状态。肥胖对全身代谢和病人预后的影响仍有争议。各种底 物诱导的表观遗传变化会改变基因表达谱，进而影响那些直接关联患者生存的代谢路径。 本文综述了 危重症中，从体重调节到免疫反应执行阶段，能量如何在体内流动的核心机制。同时也提出，未来研究应着重于受损的免疫代 谢和表观遗传机制，以期更深入理解其本质，并为危重病人带来更好的治疗预后 。 在危重症过程中，全身炎症会引发器官间特有的代谢变化。在免疫及炎症相关区域，合成代谢的重新编程主要用于支持细胞增殖和完成炎症 反应。同时，脂肪组织和骨骼肌的分解代谢为免疫和炎症细胞的合成代谢提供了必要的碳源和能量。在这些代谢调整中，肝脏至关重 ...

Core Insights - The article discusses the metabolic reprogramming that occurs during critical illness, emphasizing the role of inflammation and immune response in altering energy distribution and substrate utilization within the body [6][9][27]. Metabolic Regulation Principles - The priority of substrate utilization shifts during critical illness, with the body first consuming glucose and glycogen, followed by fats and proteins. This shift is crucial for supporting immune and inflammatory cell needs, leading to significant breakdown of muscle and fat tissues [10][13]. - The liver and kidneys enhance gluconeogenesis during critical illness, utilizing lactate, glycerol, and amino acids as substrates, which is vital for maintaining glucose levels [13]. Immune and Inflammatory Cell Metabolism - Immune cells, particularly M1 macrophages and activated T cells, primarily rely on aerobic glycolysis (Warburg effect) for rapid ATP production and biosynthetic precursors, supporting inflammatory responses despite lower energy efficiency [16][18]. - Metabolic intermediates can epigenetically regulate gene expression, influencing inflammation and immune responses [17]. Muscle and Fat Tissue Metabolic Remodeling - In critical illness, white adipose tissue may convert to brown adipose tissue, enhancing thermogenic capacity, while obesity paradox suggests that obese individuals may have better survival rates due to greater energy reserves and anti-inflammatory factors [20][22]. - Muscle protein breakdown is significantly increased due to enhanced ubiquitin-proteasome and autophagy mechanisms, leading to muscle wasting [22][26]. Conclusion - The body adapts through metabolic reprogramming during critical illness to enhance immune protection and survival, with a focus on the roles of immune cell metabolism and the breakdown of muscle and fat tissues. Future research should explore innovative interventions targeting metabolic pathways to improve clinical outcomes for critically ill patients [27].

Core Viewpoint - The article discusses the metabolic reprogramming in critically ill patients, emphasizing the importance of understanding energy flow and immune response mechanisms to improve treatment outcomes [6][9][27]. Metabolic Regulation Principles - The priority of substrate utilization in normal conditions is glucose and glycogen first, followed by fats and proteins. In critical illness, metabolism prioritizes the needs of immune and inflammatory cells, leading to significant breakdown of muscle and fat tissues to support immune cell synthesis [10][11]. - The liver and kidneys significantly enhance gluconeogenesis during critical illness, utilizing lactate, glycerol, and amino acids as substrates, with the Cori cycle playing a key role in glucose regeneration [13]. Immune and Inflammatory Cell Metabolic Reprogramming - Immune cells, such as M1 macrophages and activated T cells, primarily rely on aerobic glycolysis (Warburg effect) for rapid ATP production and biosynthetic precursors, which supports inflammatory responses but has a lower energy yield compared to mitochondrial metabolism [16][18]. - Metabolites like succinate and itaconate can regulate gene expression through epigenetic modifications, influencing inflammation and immune responses [17]. Changes in Adipose Tissue and Skeletal Muscle - In critical illness, white adipose tissue may convert to brown adipose tissue, enhancing thermogenic capacity. The "obesity paradox" suggests that obese individuals may have better survival rates in critical conditions due to greater energy reserves and anti-inflammatory factors [20]. - Muscle protein breakdown is significantly increased due to enhanced ubiquitin-proteasome and autophagy mechanisms, leading to muscle wasting and potential long-term functional impairments post-recovery [22][26]. Conclusion - The body adapts through metabolic reprogramming during critical illness to enhance immune defense and survival, with a focus on the roles of immune cell metabolism and the breakdown of skeletal muscle and adipose tissue. Future research should explore innovative interventions targeting metabolic pathways to improve clinical outcomes for critically ill patients [27].