MICROBIOLOGY AND PHYSIOLOGY OF METHANOGENESIS

我们的目标是用大鼠作为模型，研究可能 影响人类产甲烷的建立，以及 产甲烷对寄主生理的意义。产甲烷 Wistar和其他品系的大鼠的细菌将被分离和 特色化的。产甲烷菌和总活性厌氧菌将同时进行 低、中、高纤维饮食对大鼠的影响 生产CH4、H2和挥发性脂肪酸的日粮将是 量过了。产甲烷菌的建立与年龄和年龄的关系 性行为将受到调查。抗原性抗体的研究进展 将对产甲烷菌进行研究，并对大鼠进行自体免疫 确定抗体是否能消除产甲烷菌的菌株 肠子。不产甲烷的老鼠菌株将通过不同的 饮食和接种产甲烷菌株的菌群，看看是否 甲烷生成是可以建立的。 旨在测量饮食和饮食的相对贡献的实验 大肠微生物发酵的内源底物有 建议。这些措施包括使用含有营养素的基础合成饮食 完全被小肠吸收的物质。甲烷和氢气总量 生产以及添加到标签醋酸酯的稀释率 盲肠将被用来测量内源底物对 发酵。添加了以下内容后，将进行相同测量 逃脱单胃消化的底物以确定其附加值 发酵的贡献。 结果应该说明为什么甲烷是大肠的产物。 在1/3至1/2的正常成人中发酵，其余的不在发酵中 人口数量。内源底物对环境影响的评价 发酵可为使用H2和CH4的测量提供依据 生产评价差异在内生贡献中的作用 底物在不同的个体中发酵。

The goal is to use the rat as a model for studying factors that may influence the establishment of methanogenesis in humans and the significance of methanogenesis to the physiology of the host. Methanogenic bacteria of Wistar and other strains of rats will be isolated and characterized. Methanogens and total viable anaerobes will be concurrently enumeratd in rats on low, normal and high fiber diets and the influence or the diets on the production of CH4, H2 and volatile fatty acids will be measured. Establishment of methanogenic bacteria as a function of age an sex will be investigated. Development of antibodies to autochthonous methanogens will be studied and rats will be immunized with autochthonous strains to determine if antibodies cause elimination of methanogens from the intestine. Non-methanogenic rat strains will be manipulated by varying diets and inoculation with flora from methanogenic strains to see if methanogenesis can be established. Experiments designed to measure the relative contribution of dietary and endogenous substrates to large intestine microbial fermentation are proposed. These involve the use of a basal synthetic diet with nutrients that are completely absorbed in the small intestine. Total CH4 and H2 production as well as the rate of dilution of labeled acetate added to the cecum will be used to measure the contribution of endogenous substrates to fermentation. Identical measurements will be made after additions of substrates that escape monogastric digestion to determine their addtional contribution ot fermentation. The results should indicate why CH4 is a product of large intestine fermentation in 1/3 to 1/2 of normal human adults and not in the rest of the population. Evaluation of the contribution of endogenous substrates to fermentation may provide a basis for using measurements of H2 and CH4 production to evaluate differences in the contribution of endogenous substrates to fermentation in different individuals.