败血症期间细胞内氨基酸生产的急性变化与血度无关
Nicolaas E P Deutz1, Gabriella A M Ten Have2, Peter P Nghiem3
1Center for Translational Research in Aging and Longevity, Depts of Kinesiology & Sport Management, Texas A&M University, College Station, USA; Primary Care & Rural Medicine, Texas A&M University, College Station, USA.
Clinical nutrition (Edinburgh, Scotland)
|August 10, 2025
概括
早期的败血症显著改变了细胞内氨基酸代谢,池和流量的实质性变化在血度的小变化之前. 这突出了比以前理解的更复杂的代谢反应.
科学领域:
- 生物化学 生物化学
- 生理学 生理学 生理学
- 败血症病理生理学病理生理学
背景情况:
- 败血症是一种危及生命的疾病,其特点是宿主对感染的反应失调.
- 败血症的早期代谢变化尚未完全理解,特别是关于氨基酸代谢.
- 测量血氨基酸度可能无法完全捕捉发生在败血症期间的动态代谢变化.
研究的目的:
- 用猪模型研究毒症早期阶段氨基酸代谢的急性变化.
- 将血氨基酸度的变化与细胞内氨基酸池和流量进行比较.
- 阐明氨基酸代谢转变和早期败血症中血度变化之间的时间关系.
主要方法:
- 在51只猪身上使用脉冲稳定同位素追踪法来测量氨基酸的动力变化.
- 通过持续输注Pseudomonas aeruginosa引起的败血症.
- 采用分区分析来评估细胞外和细胞内氨基酸池和流量.
主要成果:
- 败血症引起了血氨基酸度的轻微 (<10%) 变化,但显著改变了氨基酸清除率.
- 分区分析揭示了细胞内氨基酸池和流量的实质性变化,通常在血度变化之前发生.
- 细胞内必需氨基酸的产生减少,而氨酸和谷氨酸的产生增加,这表明蛋白质分解和合成动态发生了变化.
结论:
- 在早期败血症期间,细胞内氨基酸代谢的显著变化迅速发生.
- 细胞内氨基酸池和流量的变化在血度的可检测变化之前.
- 对氨基酸代谢的全面评估需要的方法不仅仅是测量血度,特别是在早期的败血症.
相关概念视频
Amino Acid Biosynthetic Pathways
135
Amino acid biosynthesis is essential for cell growth, protein synthesis, and metabolic regulation. Cells generate essential and non-essential amino acids from metabolic intermediates to sustain vital biological functions. These intermediates originate from key metabolic pathways: glycolysis, the tricarboxylic acid (TCA) cycle, and the pentose phosphate pathway. Important precursors include α-ketoglutarate, pyruvate, oxaloacetate, phosphoenolpyruvate, and erythrose-4-phosphate, which...
135
Drug Distribution: Plasma Protein Binding
6.7K
Drugs predominantly attach to plasma proteins, with only a small percentage remaining unbound. The unbound portion can be calculated as one minus the bound fraction. Acidic drugs form large, inactive complexes by reversibly binding to plasma albumin, which prevents them from diffusing across biological barriers. These drug-protein complexes act as reservoirs for the drugs. As the concentration of unbound drugs decreases, these complexes quickly dissociate to release the free drug, maintaining...
6.7K
Overview of Protein Metabolism
1.8K
Proteins are broken down into amino acids during digestion. Unlike fats and carbohydrates, which are stored for later use, proteins are not. Instead, amino acids are either used to produce ATP through oxidation or contribute to the creation of new proteins for the growth and repair of the body. Any surplus amino acids from the diet are converted into glucose or triglycerides rather than excreted.
Amino acids play various roles in the body once they are absorbed into cells. They are restructured...
Amino acids play various roles in the body once they are absorbed into cells. They are restructured...
1.8K
Acute Kidney Injury II: Pathophysiology
73
Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
73
Amino Acid Catabolism
189
Microorganisms rely on proteins as an essential carbon and energy source, particularly in environments with limited polysaccharides or lipids. However, proteins are too large to cross the plasma membrane unaided, necessitating enzymatic degradation. Microbes secrete extracellular proteases and peptidases that hydrolyze proteins into peptides, which can then be transported across the membrane. Once inside the cell, intracellular proteases degrade these peptides into free amino acids, which...
189
Acute Kidney Injury III: Clinical Manifestations
94
Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...
94


