Yuan J H, Davis A J, Austic R E
Department of Animal Science, Cornell University, Ithaca, NY 14853, USA.
J Nutr. 2000 Nov;130(11):2746-52. doi: 10.1093/jn/130.11.2746.
Amino acid imbalances contribute to higher requirements of amino acids than would occur if the dietary profile of amino acids perfectly matched the requirements. The mechanisms of imbalances have not been fully elucidated. Because threonine dehydrogenase (TDH) activity in liver mitochondria increases in chicks and rats subjected to threonine imbalance, the current study was carried out to determine whether the change in TDH activity occurs rapidly enough after the consumption of an imbalanced diet to be considered a possible primary metabolic response. In a series of experiments, Leghorn chicks were allowed free access to a semipurified basal diet marginally limited in threonine or the same diet containing a mixture of indispensable amino acids (IAA) lacking threonine to cause a threonine imbalance. In the first experiment, dietary supplements of 5.5 and 11.1% IAA were used to determine a level of supplement that would cause a robust response in the specific activity of TDH. Feed intake, body weight gains and efficiency of feed utilization were lower and specific activities of TDH were higher in chicks fed 11.1% IAA than in those fed 5.5% IAA. In subsequent experiments, hepatic TDH activities and plasma amino acid profiles of the control and experimental groups were determined at 1. 5, 3, 6, 12 and 24 h after the first offering of the diet containing 11.1% IAA. The specific activities of TDH in chicks fed the IAA supplement were 40-150% higher (P < 0.05) and plasma threonine concentrations were 42-53% lower (P < 0.05) than in chicks fed the basal diet at all times except 1.5 h. These results indicate that changes in the capacity for threonine degradation via TDH may occur in the liver within a few hours after the consumption of a threonine-imbalanced diet and suggest the possibility that altered TDH activity may contribute to the increased threonine requirement associated with threonine imbalance.
与氨基酸膳食组成完全符合需求时相比，氨基酸失衡会导致对氨基酸的需求量增加。失衡的机制尚未完全阐明。由于在苏氨酸失衡的雏鸡和大鼠中，肝脏线粒体中的苏氨酸脱氢酶（TDH）活性会升高，因此开展了本研究，以确定在摄入失衡日粮后，TDH活性的变化是否足够迅速，从而被视为一种可能的主要代谢反应。在一系列实验中，让来航雏鸡自由采食一种苏氨酸含量略有限制的半纯化基础日粮，或采食相同的日粮，但添加了不含苏氨酸的必需氨基酸（IAA）混合物，以造成苏氨酸失衡。在第一个实验中，使用5.5%和11.1%的IAA日粮补充剂来确定能使TDH比活性产生强烈反应的补充剂水平。采食11.1% IAA的雏鸡的采食量、体重增加量和饲料利用效率较低，而其TDH比活性高于采食5.5% IAA的雏鸡。在随后的实验中，在首次提供含11.1% IAA的日粮后的1.5、3、6、12和24小时，测定对照组和实验组的肝脏TDH活性及血浆氨基酸谱。除1.5小时外，采食IAA补充剂的雏鸡在所有时间的TDH比活性均高出40 - 150%（P < 0.05），血浆苏氨酸浓度则低42 - 53%（P < 0.05）。这些结果表明，在摄入苏氨酸失衡日粮后的数小时内，肝脏中可能会发生通过TDH的苏氨酸降解能力变化，并提示TDH活性改变可能是导致与苏氨酸失衡相关的苏氨酸需求增加的原因。
