Carrozzo Rosalba, Torraco Alessandra, Fiermonte Giuseppe, Martinelli Diego, Di Nottia Michela, Rizza Teresa, Vozza Angelo, Verrigni Daniela, Diodato Daria, Parisi Giovanni, Maiorana Arianna, Rizzo Cristiano, Pierri Ciro Leonardo, Zucano Stefania, Piemonte Fiorella, Bertini Enrico, Dionisi-Vici Carlo
Unit of Molecular Medicine for Neuromuscular and Neurodegenerative Diseases, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
Unit of Molecular Medicine for Neuromuscular and Neurodegenerative Diseases, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
Mitochondrion. 2014 Sep;18:49-57. doi: 10.1016/j.mito.2014.09.006. Epub 2014 Sep 22.
Dihydrolipoamide dehydrogenase (DLD, E3) is a flavoprotein common to pyruvate, α-ketoglutarate and branched-chain α-keto acid dehydrogenases. We found two novel DLD mutations (p.I40Lfs*4; p.G461E) in a 19 year-old patient with lactic acidosis and a complex amino- and organic aciduria consistent with DLD deficiency, manifesting progressive exertional fatigue. Muscle biopsy showed mitochondrial proliferation and lack of DLD cross-reacting material. Riboflavin supplementation determined the complete resolution of exercise intolerance with the partial restoration of the DLD protein and disappearance of mitochondrial proliferation in the muscle. Morphological and functional studies support the riboflavin chaperon-like role in stabilizing DLD protein with rescue of its expression in the muscle.
二氢硫辛酰胺脱氢酶(DLD,E3)是一种存在于丙酮酸、α-酮戊二酸和支链α-酮酸脱氢酶中的黄素蛋白。我们在一名19岁患有乳酸酸中毒且伴有与DLD缺乏症相符的复杂氨基酸尿和有机酸尿的患者中发现了两个新的DLD突变(p.I40Lfs*4;p.G461E),该患者表现为进行性运动性疲劳。肌肉活检显示线粒体增殖且缺乏DLD交叉反应物质。补充核黄素后,运动不耐受完全缓解,肌肉中DLD蛋白部分恢复,线粒体增殖消失。形态学和功能研究支持核黄素具有类似伴侣蛋白的作用,可稳定DLD蛋白并使其在肌肉中的表达得以恢复。