Choline, an essential nutrient for humans.
Choline, an essential nutrient for humans.
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DOI：
10.1016/s0899-9007(00)00349-x
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发表时间：
2000-07
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影响因子：
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通讯作者：
Steven;-H.;ZEISEL’;Kerry-Ann;DA Costa;Peter;-D.;Franklin;Edward;-A.;Alexander;-J.;Thomas;Lamont;Nancy;F. Sheard;Alexa;Beiser
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文献类型：
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作者：
Steven;-H.;ZEISEL’;Kerry-Ann;DA Costa;Peter;-D.;Franklin;Edward;-A.;Alexander;-J.;Thomas;Lamont;Nancy;F. Sheard;Alexa;Beiser
胆碱是细胞膜中磷脂合成、甲基代谢、胆碱能神经传递、跨膜信号传导和脂质-胆固醇转运和代谢所必需的。胆碱可以被乙酰化、磷酸化、氧化或水解。有几个全面的审查的代谢和功能的胆碱。1-3毫无疑问，细胞绝对需要胆碱，当缺乏这种营养时，细胞会因凋亡而死亡。5-7关于人类饮食是否必须含有胆碱的争论之所以出现，是因为存在一种途径（在肝脏中最活跃），通过使用S-腺苷甲硫氨酸作为甲基供体的磷脂酰乙醇胺的顺序甲基化来从头生物合成胆碱部分。这种从头形成胆碱部分的能力意味着对胆碱的一些需求可以部分地通过使用来自一碳代谢的甲基（通过甲基叶酸和甲硫氨酸）来满足。由于胆碱、甲硫氨酸、叶酸、维生素B6和B12的这种代谢相互关系，研究人员需要证明，当其他营养素的量足以维持正常的生长和功能时，在胆碱被指定为必需品之前，从头合成速率不足以满足对胆碱的需求。包括狒狒在内的许多动物，如果饮食中缺乏胆碱，就会耗尽体内的胆碱储备，从而导致肝功能障碍。9-13动物喂养胆碱缺乏的饮食也可能发展生长迟缓，肾功能不全和出血，或骨骼异常。12，14，15毫无疑问，许多哺乳动物需要胆碱，因此胆碱通常被添加到动物饲料中。一些人（男性和女性）用不含胆碱但足以提供蛋氨酸和叶酸的全肠外营养（TPN）溶液喂养，会出现脂肪肝和肝损伤，当提供胆碱来源时，这些症状会得到缓解。16-21脂肪肝的发生是因为需要胆碱来制造极低密度脂蛋白（VLDL）颗粒的磷脂酰胆碱部分。[22，23]在缺乏胆碱的情况下，VLDL不被分泌，三酰甘油在肝细胞质中积累。Buchman及其同事16对TPN患者口服卵磷脂（30%磷脂酰胆碱）。6周后，卵磷脂组的血浆胆碱增加了50%，而安慰剂组减少了25%。在治疗组中，肝脏脂肪减少了30%。在其他研究中，静脉注射氯化胆碱同样有效。17这些TPN研究的数据支持这样的结论，即胆碱的从头合成并不总是足以满足人类对胆碱的需要。
Choline is needed for synthesis of the phospholipids in cell membranes, methyl metabolism, cholinergic neurotransmission, transmembrane signaling, and lipid-cholesterol transport and metabolism. 1 Choline can be acetylated, phosphorylated, oxidized, or hydrolyzed. There are several comprehensive reviews of the metabolism and functions of choline. 1–3 There is no doubt that cells absolutely require choline, 4 and die by apoptosis when deprived of this nutrient. 5–7 The debate as to whether the human diet must contain choline arises because there is a pathway (most active in the liver) for the de novo biosynthesis of the choline moiety via the sequential methylation of phosphatidylethanolamine using S-adenosylmethionine as the methyl donor. 8 This ability to form choline moiety de novo means that some of the demand for choline can, in part, be met by using methylgroups derived from one-carbon metabolism (via methyl-folate and methionine). Because of this metabolic interrelationship of choline, methionine, folate, and vitamins B6 and B12, investigators need to show that, when the other nutrients are available in amounts sufficient to sustain normal growth and function, de novo synthesis rates are not adequate to meet the demand for choline before the designation of choline as essential is made. Many species of animals, including the baboon, fed a cholinedeficient diet deplete choline stores and develop liver dysfunction. 9–13 Animals fed a choline-deficient diet may also develop growth retardation, renal dysfunction and hemorrhage, or bone abnormalities. 12, 14, 15 There is no question that many mammals require dietary choline, and for this reason choline is usually added to animal feeds.Some humans (male and female) fed with total parenteral nutrition (TPN) solutions devoid of choline, but adequate for methionine and folate, develop fatty liver and liver damage that resolves when a source of dietary choline is provided. 16–21 Fatty liver occurs because choline is required to make the phosphatidylcholine portion of the very low-density lipoprotein (VLDL) particle. 22, 23 In the absence of choline, VLDL is not secreted and triacylglyerol accumulates in hepatic cytosol. Buchman and colleagues16 administered lecithin (30% phosphatidylcholine) orally to TPN patients. After 6 wk, plasma choline increased by 50% in the lecithin group, whereas in the placebo group it had decreased by 25%. In the treated group, liver fat decreased by 30%. In other studies, intravenous choline chloride was just as effective. 17 The data from these TPN studies support the conclusion that de novo synthesis of choline is not always sufficient to meet human requirements for choline.