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首页> 外文会议>International Symposium on the Nutrition of Herbivores(ISNH-7); 20070917-22; Beijing(CN) >Host and intestinal microbiota negotiations in the context of animal growth efficiency
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Host and intestinal microbiota negotiations in the context of animal growth efficiency

机译：在动物生长效率方面的宿主和肠道微生物群谈判

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That bacterial colonization of the intestine negatively impacts the efficiency of animal growth is well documented through data from studies with germfree (GF) animals, and by increasing evidence that the growth enhancing effects of antibiotics likely reflect their ability to both decrease intestinal bacterial colonization and alter community profiles. For example, oral antibiotics do not induce a growth-response in GF animals (Coates et al., 1963), while colonizing GF animals with normal intestinal bacteria depresses growth (Coates, 1980). Growth depression is thought to result from the increased maintenance costs associated with host responses to the variety of catabolic processes that mediate bacterial growth in the intestine (Gaskins, 2001). However, quantitative data to support or refute that concept are limited.nHost sensitivity to the intestinal microbiota is further suggested by parallel developmental and regional differences in intestinal structure and function and microbial density, as well as the reduction in epithelial cell turnover and intestinal secretory activity in GF animals. Thus, regulatory cues must exist that enable the host to monitor the extent of bacterial colonization and activity. If this is so, then opportunities should exist for improving animal growth efficiency through the manipulation of the dynamic equilibrium between the intestinal microbiota and host defense functions. These issues raise the important point that while there is presumably a microbiota that optimizes intestinal health, the maintenance of this population becomes part of the nutrient requirements of the host and thereby affects whole body growth efficiency.
机译：通过对无菌（GF）动物的研究数据以及越来越多的证据表明，抗生素的生长促进作用很可能反映出它们减少肠道细菌定殖和改变的能力，充分证明了肠道细菌定殖会对动物生长效率产生负面影响。社区资料。例如，口服抗生素不会在GF动物中诱导生长反应（Coates等，1963），而在GF动物中掺入正常肠道细菌会抑制生长（Coates，1980）。生长抑制被认为是由于宿主对介导细菌在肠道中生长的各种分解代谢过程的反应而导致的维护成本增加所致（Gaskins，2001）。然而，支持或驳斥该概念的定量数据有限.n肠道结构，功能和微生物密度的平行发育和区域差异以及上皮细胞更新和肠道分泌活性的降低进一步提示了宿主对肠道菌群的敏感性。在GF动物中。因此，必须存在使宿主能够监测细菌定殖和活性程度的调控信号。如果是这样，那么应该存在通过控制肠道菌群和宿主防御功能之间动态平衡来改善动物生长效率的机会。这些问题提出了一个重要的观点，即虽然可能存在一种优化肠道健康的微生物群，但维持这一种群成为宿主营养需求的一部分，从而影响了整个人体的生长效率。

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