Hughes Juliette H, Wilson Peter J M, Sutherland Hazel, Judd Shirley, Hughes Andrew T, Milan Anna M, Jarvis Jonathan C, Bou-Gharios George, Ranganath Lakshminarayan R, Gallagher James A
Department of Musculoskeletal Biology I, Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, UK.
Department of Nutrition and Dietetics, Royal Liverpool University Hospital Trust, Liverpool, UK.
J Inherit Metab Dis. 2020 Mar;43(2):259-268. doi: 10.1002/jimd.12172. Epub 2020 Jan 13.
Alkaptonuria (AKU) is caused by homogentisate 1,2-dioxygenase deficiency that leads to homogentisic acid (HGA) accumulation, ochronosis and severe osteoarthropathy. Recently, nitisinone treatment, which blocks HGA formation, has been effective in AKU patients. However, a consequence of nitisinone is elevated tyrosine that can cause keratopathy. The effect of tyrosine and phenylalanine dietary restriction was investigated in nitisinone-treated AKU mice, and in an observational study of dietary intervention in AKU patients. Nitisinone-treated AKU mice were fed tyrosine/phenylalanine-free and phenylalanine-free diets with phenylalanine supplementation in drinking water. Tyrosine metabolites were measured pre-nitisinone, post-nitisinone, and after dietary restriction. Subsequently an observational study was undertaken in 10 patients attending the National Alkaptonuria Centre (NAC), with tyrosine >700 μmol/L who had been advised to restrict dietary protein intake and where necessary, to use tyrosine/phenylalanine-free amino acid supplements. Elevated tyrosine (813 μmol/L) was significantly reduced in nitisinone-treated AKU mice fed a tyrosine/phenylalanine-free diet in a dose responsive manner. At 3 days of restriction, tyrosine was 389.3, 274.8, and 144.3 μmol/L with decreasing phenylalanine doses. In contrast, tyrosine was not effectively reduced in mice by a phenylalanine-free diet; at 3 days tyrosine was 757.3, 530.2, and 656.2 μmol/L, with no dose response to phenylalanine supplementation. In NAC patients, tyrosine was significantly reduced (P = .002) when restricting dietary protein alone, and when combined with tyrosine/phenylalanine-free amino acid supplementation; 4 out of 10 patients achieved tyrosine <700 μmol/L. Tyrosine/phenylalanine dietary restriction significantly reduced nitisinone-induced tyrosinemia in mice, with phenylalanine restriction alone proving ineffective. Similarly, protein restriction significantly reduced circulating tyrosine in AKU patients.
黑尿症(AKU)是由尿黑酸1,2 -双加氧酶缺乏引起的,该缺乏会导致尿黑酸(HGA)积累、褐黄病和严重的骨关节炎。最近,阻断HGA形成的尼替西农治疗对AKU患者有效。然而,尼替西农的一个后果是酪氨酸升高,这可能导致角膜病变。在接受尼替西农治疗的AKU小鼠以及一项关于AKU患者饮食干预的观察性研究中,对酪氨酸和苯丙氨酸饮食限制的效果进行了研究。给接受尼替西农治疗的AKU小鼠喂食不含酪氨酸/苯丙氨酸的饮食以及不含苯丙氨酸但在饮用水中补充苯丙氨酸的饮食。在尼替西农治疗前、治疗后以及饮食限制后测量酪氨酸代谢产物。随后,对10名就诊于国家黑尿症中心(NAC)的患者进行了一项观察性研究,这些患者的酪氨酸>700 μmol/L,他们已被建议限制饮食蛋白质摄入量,并在必要时使用不含酪氨酸/苯丙氨酸的氨基酸补充剂。在喂食不含酪氨酸/苯丙氨酸饮食的接受尼替西农治疗的AKU小鼠中,升高的酪氨酸(813 μmol/L)以剂量反应方式显著降低。在限制饮食3天时,随着苯丙氨酸剂量减少,酪氨酸分别为389.3、274.8和144.3 μmol/L。相比之下,不含苯丙氨酸的饮食未能有效降低小鼠体内的酪氨酸;在3天时,酪氨酸分别为757.3、53 and 656.2 μmol/L,对苯丙氨酸补充无剂量反应。在NAC患者中,单独限制饮食蛋白质以及与不含酪氨酸/苯丙氨酸的氨基酸补充剂联合使用时,酪氨酸显著降低(P = 0.002);10名患者中有4名的酪氨酸<700 μmol/L。酪氨酸/苯丙氨酸饮食限制显著降低了尼替西农诱导的小鼠酪氨酸血症,而单独限制苯丙氨酸证明无效。同样,蛋白质限制显著降低了AKU患者循环中的酪氨酸水平。