Exercise modifies glutamate and other metabolic biomarkers in cerebrospinal fluid from Gulf War Illness and Myalgic encephalomyelitis / Chronic Fatigue Syndrome.
Exercise modifies glutamate and other metabolic biomarkers in cerebrospinal fluid from Gulf War Illness and Myalgic encephalomyelitis / Chronic Fatigue Syndrome.
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DOI：
10.1371/journal.pone.0244116
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发表时间：
2021
期刊：
影响因子：
3.7
通讯作者：
Cheema A
中科院分区：
文献类型：
--
作者：
Baraniuk JN;Kern G;Narayan V;Cheema A
肌痛性脑脊髓炎/慢性疲劳综合征（ME/CFS）和海湾战争病（GWI）有许多共同的疲劳，疼痛和认知功能障碍症状，这些症状不能通过休息来缓解。ME/CFS和GWI的血清代谢物模式与对照组不同，提示可能存在能量和脂质代谢障碍。在（a）休息或（B）次极量运动负荷试验后进行腰椎穿刺的2组受试者中，比较ME/CFS、GWI和久坐对照组的脑脊液代谢组学。根据获得性短暂性运动后姿势性心动过速对运动后GWI和对照受试者进行细分。使用Biocrates AbsoluteIDQ® p180试剂盒对储存的脑脊液标本进行分析，用于氨基酸、胺、酰基肉毒碱、鞘脂、溶血磷脂、烷基和醚磷酸胆碱的定量靶向代谢组学研究。与非运动组和其他运动后组相比，运动后未发生体位性心动过速的运动后GWI受试者亚组的谷氨酸盐显著升高。非运动组之间的唯一差异是GWI中的lysoPC a C28：0高于ME/CFS，这表明这种生化或磷脂酶活性可能具有作为区分这两种疾病的生物标志物的潜力。运动后对照组短链酰基肉毒碱C5-OH（C3-DC-M）水平高于非运动ME/CFS组。局限性包括亚组样本量小和缺乏运动后ME/CFS标本。谷氨酸神经兴奋性毒性的机制可能有助于神经病理学和“神经炎症”的GWI子集谁没有开发运动后体位性心动过速。脂质代谢功能障碍可以区分主要为女性的ME/CFS组与主要为男性的GWI受试者。
Myalgic encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS) and Gulf War Illness (GWI) share many symptoms of fatigue, pain, and cognitive dysfunction that are not relieved by rest. Patterns of serum metabolites in ME/CFS and GWI are different from control groups and suggest potential dysfunction of energy and lipid metabolism. The metabolomics of cerebrospinal fluid was contrasted between ME/CFS, GWI and sedentary controls in 2 sets of subjects who had lumbar punctures after either (a) rest or (b) submaximal exercise stress tests. Postexercise GWI and control subjects were subdivided according to acquired transient postexertional postural tachycardia. Banked cerebrospinal fluid specimens were assayed using Biocrates AbsoluteIDQ® p180 kits for quantitative targeted metabolomics studies of amino acids, amines, acylcarnitines, sphingolipids, lysophospholipids, alkyl and ether phosphocholines. Glutamate was significantly higher in the subgroup of postexercise GWI subjects who did not develop postural tachycardia after exercise compared to nonexercise and other postexercise groups. The only difference between nonexercise groups was higher lysoPC a C28:0 in GWI than ME/CFS suggesting this biochemical or phospholipase activities may have potential as a biomarker to distinguish between the 2 diseases. Exercise effects were suggested by elevation of short chain acylcarnitine C5-OH (C3-DC-M) in postexercise controls compared to nonexercise ME/CFS. Limitations include small subgroup sample sizes and absence of postexercise ME/CFS specimens. Mechanisms of glutamate neuroexcitotoxicity may contribute to neuropathology and “neuroinflammation” in the GWI subset who did not develop postural tachycardia after exercise. Dysfunctional lipid metabolism may distinguish the predominantly female ME/CFS group from predominantly male GWI subjects.
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