Threonine-deficient diets induced changes in hepatic bioenergetics
Threonine-deficient diets induced changes in hepatic bioenergetics
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DOI：
10.1152/ajpgi.90545.2008
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发表时间：
2009-05-01
影响因子：
4.5
通讯作者：
Giulivi, Cecilia
中科院分区：
文献类型：
--
作者：
Ross-Inta, Catherine M.;Zhang, Yi-Fan;Giulivi, Cecilia
Ross-Inta CM，Zhang Y-F，Almendares A，Giulivi C。苏氨酸缺乏饮食诱导肝脏生物能学变化。 Am J Physiol Gastrointest Liver Physiol 296：G1130-G1139，2009。首次发表于 2009 年 2 月 19 日； doi:10.1152/ajpgi.90545.2008.-已知缺乏必需氨基酸的饮食会抑制大鼠的食物摄入。很少有研究关注于了解缺乏氨基酸的饮食如何引起线粒体水平的生化变化。本研究的目的是评估饲喂含有 0.00、0.18、0.36 和 0.88% 苏氨酸 (Thr) 饮食的大鼠的线粒体功能（设定为生长所需 Thr 的 0、30、60 和 140%）。在此，首次描述了缺乏 Thr 的饮食会诱导肝脏中线粒体的特异性解偶联，尤其是与 NADH 连接的底物，而在心脏中未观察到（除了缺乏 Thr 的饮食）。这种情况的优点是，当可以获得高质量蛋白质食物（或一般来说大量的高质量食物）时，可以提供 ATP 来支持生长和维持，而缺乏 Thr 的饮食（或缺乏质量蛋白质食物）则会促进相反的情况，增加肝脏中的线粒体解偶联。与 NADH 底物的解偶联有利于使用具有较高 FADH 与 NADH 比率的营养物质作为能源，例如脂肪，最大限度地减少许多氨基酸（包括苏氨酸）的首次不可逆 NADH 依赖性分解代谢，从而在低质量蛋白质来源可用时增强限制性氨基酸在蛋白质合成中的使用。
Ross-Inta CM, Zhang Y-F, Almendares A, Giulivi C. Threonine-deficient diets induced changes in hepatic bioenergetics. Am J Physiol Gastrointest Liver Physiol 296: G1130-G1139, 2009. First published February 19, 2009; doi:10.1152/ajpgi.90545.2008.-Diets deficient in an indispensable amino acid are known to suppress food intake in rats. Few studies were focused at understanding how amino acid-deficient diets may elicit biochemical changes at the mitochondrial level. The goal of this study was to evaluate mitochondrial function in rats fed diets with 0.00, 0.18, 0.36, and 0.88% threonine (Thr) (set at 0, 30, 60, and 140% of Thr requirement for growth). Here, it is described for the first time that Thr-deficient diets induce a specific uncoupling of mitochondria in liver, especially with NADH-linked substrates, not observed in heart (except for Thr-devoid diet). The advantage of this situation would be to provide ATP to support growth and maintenance when high-quality protein food (or wealth of high- quality food in general) is available, whereas Thr-deficient diets (or deficient-quality protein food) promote the opposite, increasing mitochondrial uncoupling in liver. The uncoupling with NADH substrates would favor the use of nutrients as energy sources with higher FADH-to-NADH ratios, such as fat, minimizing the first irreversible NADH-dependent catabolism of many amino acids, including Thr, thus enhancing the use of the limiting amino acid for protein synthesis when a low quality protein source is available.