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糖蛋白作为结肠细菌菌群产生氢气和甲烷的底物。

Glycoproteins as substrates for production of hydrogen and methane by colonic bacterial flora.

作者信息

Perman J A, Modler S

出版信息

Gastroenterology. 1982 Aug;83(2):388-93.

PMID:7084616
Abstract

Hydrogen and methane in human breath derive entirely from bacterial fermentation in the intestinal lumen. The sources of substrates utilized for these reactions have not been completely determined. Basal excretion of both gases occurs in the fasted state, while malabsorbed carbohydrate commonly results in increased hydrogen but not methane production. Using an in vitro fecal incubation system, we have studied hydrogen and methane production from glycoproteins of endogenous as well as dietary origin. All glycoproteins tested yielded hydrogen when incubated with fecal homogenates. Mean hydrogen production from substrates containing less than 3% sugar (human serum albumin, bovine serum albumin, and alpha-casein) averaged 2.2 +/- 0.9% of hydrogen production from equivalent amounts of glucose, while carbohydrate-rich mucin yielded 46.0 +/- 6.7% of hydrogen production from glucose. Glycoproteins of intermediate carbohydrate content, including transferrin and egg white, yielded intermediate values. Methane production from glycoproteins was optimal from carbohydrate-poor protein substrates in fecal homogenates which accumulated hydrogen and became rapidly acidic when incubated with pure carbohydrate. In contrast, methane production was comparable for essentially sugar-free proteins, glycoproteins, and glucose when hydrogen did not accumulate and neutral pH was maintained. We conclude that glycoproteins are substrates for hydrogen and methane production by colonic bacteria from healthy adults. In individuals with bacterial overgrowth syndromes and in protein-losing enteropathy, bacterial catabolism of endogenous glycoproteins may cause increased basal hydrogen and methane excretion. These findings also raise the possibility that measurement of hydrogen or methane after oral administration of dietary glycoproteins may be useful in detection of protein malabsorption.

摘要

人体呼出气体中的氢气和甲烷完全源自肠腔内的细菌发酵。这些反应所利用的底物来源尚未完全明确。禁食状态下会出现这两种气体的基础排泄,而碳水化合物吸收不良通常会导致氢气生成增加,但不会导致甲烷生成增加。我们使用体外粪便培养系统,研究了内源性以及饮食来源的糖蛋白产生氢气和甲烷的情况。所有测试的糖蛋白与粪便匀浆一起孵育时都会产生氢气。含糖量低于3%的底物(人血清白蛋白、牛血清白蛋白和α-酪蛋白)产生的氢气平均量为等量葡萄糖产生氢气量的2.2±0.9%,而富含碳水化合物的粘蛋白产生的氢气量为葡萄糖产生氢气量的46.0±6.7%。碳水化合物含量中等的糖蛋白,包括转铁蛋白和蛋清,产生的氢气量处于中间值。在粪便匀浆中,贫碳水化合物的蛋白质底物产生甲烷的情况最佳,这些底物在与纯碳水化合物孵育时会积累氢气并迅速变酸。相比之下,当不积累氢气并维持中性pH值时,基本无糖的蛋白质、糖蛋白和葡萄糖产生甲烷的情况相当。我们得出结论,糖蛋白是健康成年人结肠细菌产生氢气和甲烷的底物。在患有细菌过度生长综合征和蛋白丢失性肠病的个体中,内源性糖蛋白的细菌分解代谢可能会导致基础氢气和甲烷排泄增加。这些发现还增加了一种可能性,即口服饮食糖蛋白后测量氢气或甲烷可能有助于检测蛋白质吸收不良。

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