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首页> 外文期刊>Medical hypotheses >Suggested pathology of systemic exertion intolerance disease: Impairment of the E-3 subunit or crossover of swinging arms of the E-2 subunit of the pyruvate dehydrogenase complex decreases regeneration of cofactor dihydrolipoic acid of the E-2 subunit
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Suggested pathology of systemic exertion intolerance disease: Impairment of the E-3 subunit or crossover of swinging arms of the E-2 subunit of the pyruvate dehydrogenase complex decreases regeneration of cofactor dihydrolipoic acid of the E-2 subunit

机译：建议的全身劳累不耐受疾病的病理：丙酮酸脱氢酶复合酶复合酶复合酶复合物的E-2亚基的e-2亚基摆动的损伤或交叉的损伤降低了E-2亚基的辅因子二氢甲酸的再生

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Systemic Exertion Intolerance Disease (SEID) or myalgic encephalomyelitis (ME) or chronic fatigue syndrome (CFS) has an unknown aetiology, with no known treatment and a prevalence of approximately 22 million individuals (2%) in Western countries. Although strongly suspected, the role of lactate in pathology is unknown, nor has the nature of the two most central symptoms of the condition post exertional malaise and fatigue. The proposed mechanism of action of pyruvate dehydrogenase complex (PDC) plays a central role in maintaining energy production with cofactors alpha-lipoic acid (LA) and its counterpart dihydrolipoic acid (DHLA), its regeneration suggested as the new rate limiting factor. Decreased DHLA regeneration due to impairment of the E-3 subunit or crossover of the swinging arms of the E-2 subunit of PDC have been suggested as a cause of ME/CFS/SEID resulting in instantaneous fluctuations in lactate levels and instantaneous offset of the DHLA/LA ratio and defining the condition as an LA deficiency with chronic instantaneous hyperlactataemia with explicit stratification of symptoms. While instantaneous hyperlactataemia has been suggested to account for the PEM, the fatigue was explained by the downregulated throughput of pyruvate and consequently lower production of ATP with the residual enzymatic efficacy of the E-3 subunit or crossover of the E-2 as a proposed explanation of the fatigue severity. Functional diagnostics and visualization of instantaneous elevations of lactate and DHLA has been suggested. Novel treatment strategies have been implicated to compensate for chronic PDC impairment and hyperlactataemia. This hypothesis potentially influences the current understanding and treatment methods for any type of hyperlactataemia, fatigue, ME/CFS/SEID, and conditions associated with PDC impairment.
机译：全身劳累的不耐受性疾病（SEID）或肌间脑脊髓炎（ME）或慢性疲劳综合征（CFS）具有未知的疾病，无知的治疗和西方国家约2200万人（2％）的患病率。虽然强烈怀疑，但乳酸在病理学中的作用是未知的，也不是具有疲劳性能术后的两种最中心症状的性质。所提出的丙酮酸脱氢酶复合物（PDC）的作用机制在将能量产生与辅助actorsα-硫辛酸（LA）和其对应二氢甲酸（DHLA）保持能量产生方面起着核心作用，其再生表明是新的速率限制因子。由于E-3亚基的损害而减少了DHLA再生或PDC的E-2亚基的摆动臂的交叉作为ME / CFS / SEID的原因，导致乳酸水平瞬时波动和瞬时偏移DHLA / LA比和定义慢性瞬时高级性血症的LA缺乏，明确分层症状。虽然已经提出瞬时高级性血症来占PEM，但通过丙酮酸的下调产量，并以e-3亚基的残留酶促效果或e-2的交叉作为提出的解释，解释疲劳疲劳严重程度。提出了乳酸和DHLA瞬时升高的功能诊断和可视化。新颖的治疗策略涉及弥补慢性PDC损伤和高结血症的补偿。该假设可能对任何类型的高级病毒血症，疲劳，ME / CFS / SEID和与PDC障碍相关的条件影响目前的理解和治疗方法。

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