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    目前服用他汀類(lèi)藥物治療高膽固醇癥的病人或許會(huì )存在肌肉疼痛，近日，來(lái)自哥本哈根大學(xué)的研究者發(fā)現了病人出現肌肉疼痛癥狀的內在機制，相關(guān)研究成果刊登在了國際雜志Journal of American College of Cardiology上。

    他汀類(lèi)藥物（statin）是一類(lèi)通過(guò)抑制肝臟產(chǎn)生膽固醇的能力來(lái)治療血液中高膽固醇的藥物，其是市場(chǎng)上最有潛力的降低低密度脂蛋白的藥物，目前將近有600，000名丹麥人每天服用該類(lèi)藥物來(lái)治療高膽固醇癥。

    研究者Flemming Dela教授表示，我們都知道服用他汀類(lèi)藥物會(huì )引發(fā)肌肉疼痛，而且有75%的病人都經(jīng)歷著(zhù)疼痛的折磨，如今我們的研究揭示了他汀類(lèi)藥物療法可以影響肌肉能量的產(chǎn)生，這或許是直接導致病人肌肉虛弱和疼痛的原因。

    研究中，研究者同樣揭示了進(jìn)行他汀類(lèi)藥物療法的患者體內或許關(guān)鍵蛋白Q10的水平較低，肌肉中Q10的好進(jìn)以及隨既而來(lái)的低能量產(chǎn)生會(huì )許是引發(fā)許多病人肌肉疼痛的主要原因。在丹麥大約40%的病人進(jìn)行他汀類(lèi)藥物療法稱(chēng)為mono療法，而且這僅僅是患高膽固醇病人使用的療法，而且這些病人并沒(méi)有其它影響心臟健康的風(fēng)險因素。

    在研究中，研究者以患者他汀類(lèi)藥物療法為視角調查了其對病人的影響，結果發(fā)現接受他汀類(lèi)藥物療法的病人，使用該療法會(huì )影響其機體肌肉的能量代謝，從而導致患者出現肌肉疼痛癥狀，這就為研究者深入研究其發(fā)病機制提供了思路和線(xiàn)索。

    Simvastatin Effects on Skeletal Muscle : Relation to Decreased Mitochondrial Function and Glucose Intolerance

    Objectives: Glucose tolerance and skeletal muscle coenzyme Q10 (Q10) content, mitochondrial density, and mitochondrial oxidative phosphorylation (OXPHOS) capacity were measured in simvastatin-treated patients (n = 10) and in well-matched control subjects (n = 9).

    Background: A prevalent side effect of statin therapy is muscle pain, and yet the basic mechanism behind it remains unknown. We hypothesize that a statin-induced reduction in muscle Q10 may attenuate mitochondrial OXPHOS capacity, which may be an underlying mechanism.

    Methods: Plasma glucose and insulin concentrations were measured during an oral glucose tolerance test. Mitochondrial OXPHOS capacity was measured in permeabilized muscle fibers by high-resolution respirometry in a cross-sectional design. Mitochondrial content (estimated by citrate synthase [CS] activity, cardiolipin content, and voltage-dependent anion channel [VDAC] content) as well as Q10 content was determined.

    Results: Simvastatin-treated patients had an impaired glucose tolerance and displayed a decreased insulin sensitivity index. Regarding mitochondrial studies, Q10 content was reduced (p = 0.05), whereas mitochondrial content was similar between the groups. OXPHOS capacity was comparable between groups when complex I– and complex II–linked substrates were used alone, but when complex I + II–linked substrates were used (eliciting convergent electron input into the Q intersection [maximal ex vivo OXPHOS capacity]), a decreased (p < 0.01) capacity was observed in the patients compared with the control subjects.

    Conclusions: These simvastatin-treated patients were glucose intolerant. A decreased Q10 content was accompanied by a decreased maximal OXPHOS capacity in the simvastatin-treated patients. It is plausible that this finding partly explains the muscle pain and exercise intolerance that many patients experience with their statin treatment.