Contribution of microbial amino acids to amino acid homeostasis of the host
Contribution of microbial amino acids to amino acid homeostasis of the host
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DOI：
10.1093/jn/130.7.1857s
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发表时间：
2000-07-01
影响因子：
4.2
通讯作者：
Metges, CC
中科院分区：
文献类型：
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作者：
Metges, CC
氮平衡和示踪剂来源的必需氨基酸（IAA）需求估计值之间的差异的原因之一是，代谢的要求不仅是由饮食，但也由IAA从头合成的胃肠道微生物群落，然后吸收的可能性。因此，更好地了解和量化人体胃肠道中氨基酸的微生物生物合成及其在提供IAA以满足人体氨基酸需求方面的潜在作用至关重要。在这里，微生物氨基酸对宿主的氨基酸稳态的贡献，应用N-15标记的范例，现有的证据进行了总结。宿主的循环血浆赖氨酸、尿赖氨酸和体蛋白赖氨酸的1 - 20%分别来自肠微生物来源，对应于11-68 mg的总微生物赖氨酸贡献。kg（-1）。d（-1）在具有足够蛋白质摄入的成年人中，当粪便或回肠微生物赖氨酸富集用作前体时。影响净微生物IAA贡献估计的因素进行了讨论。看来小肠负责大部分的微生物赖氨酸摄取，尽管不能排除来自大肠的一些吸收。从人胃肠道的非氧化赖氨酸损失，发现在3.9至8.5 mg之间。kg（-1）。d（-1），是估算微生物IAA净贡献所必需的。合理的假设是，人胃肠道中的微生物氨基酸合成利用各种氮源的混合物，即，内源性氨基酸、尿素和氨。小肠中的微生物可能更多地依赖于内源性氨基酸。营养素的去除、某些膳食非淀粉寡糖、脂质的摄入以及蛋白质摄入水平和某些氨基酸的来源和消耗水平可以影响肠道微生物群落的组成和代谢活性，从而影响宿主可能获得的其发酵产物。总之，通过使用N-15标记范例，发现微生物赖氨酸对宿主赖氨酸稳态的显著贡献。然而，为了评估微生物IAA的净贡献及其在确定成虫IAA需要量中的重要性，这不是最终成功的实验策略，因为结果的解释被肠道中的氮循环复杂化，前体吸收池的不确定性和人体胃肠道非氧化性IAA损失的有限数据。
Among the reasons suggested for the discrepancy between N balance and tracer-derived indispensable amino acid (IAA) requirement estimates is the possibility that the metabolic requirement is met not only by the diet but also by IAA synthesized de novo by the gastrointestinal microflora, which are then absorbed. It is therefore crucial to better understand and quantify the microbial biosynthesis of amino acids in the human gastrointestinal tract and its potential role in providing IAA to meet human amino acid requirement. Here, the available evidence on the contribution of microbial amino acids to the host's amino acid homeostasis, applying the N-15 labeling paradigm, is summarized. Between 1 and 20% of circulating plasma lysine, urinary lysine and body protein lysine of the host, respectively, is derived from intestinal microbial sources and corresponds to a gross microbial lysine contribution of 11-68 mg . kg(-1) . d(-1) in adult humans with an adequate protein intake when fecal or ileal microbial lysine enrichment is used as precursor. Factors affecting estimates of net microbial IAA contribution are discussed. It appears that the small intestine is responsible for a large part of microbial lysine uptake, although some absorption from the large intestine cannot be excluded. Nonoxidative lysine losses from the human gastrointestinal tract, which were found to be between 3.9 to 8.5 mg . kg(-1) . d(-1), are necessary to estimate the net contribution of microbial IAA. It is reasonable to assume that microbial amino acid synthesis in the human gastrointestinal tract utilizes a mixture of various nitrogen sources, i.e., endogenous amino acids, urea and ammonia. Microbes in the small intestine may rely more on endogenous amino acids. Deprivation of nutrients, the intake of certain dietary nonstarch oligosaccharides, lipids, as well as protein intake level and source and level of consumption of certain amino acids can affect the composition and metabolic activity of the intestinal microflora and thus its fermentation products potentially available to the host. In conclusion, with the use of the N-15 labeling paradigm, a significant contribution of microbial lysine to the host lysine homeostasis is found. However, to assess the net contribution of microbial IAA and its importance in defining the adult IAA requirement, this is not the ultimately successful experimental strategy because the interpretation of results is complicated by the nitrogen recycling in the gut, the uncertainty of the precursor pool of absorption and the limited data on nonoxidative IAA losses from the human gastrointestinal tract.