Chaturvedi P, Warren C D, Buescher C R, Pickering L K, Newburg D S
Shriver Center, Waltham, MA, USA.
Adv Exp Med Biol. 2001;501:315-23. doi: 10.1007/978-1-4615-1371-1_39.
Several human milk oligosaccharides inhibit human pathogens in vitro and in animal models. In an infant, the ability of these oligosaccharides to offer protection from enteric pathogens would require that they withstand structural modification as they pass through the alimentary canal or are absorbed and excreted in urine. We investigated the fate of human milk oligosaccharides during transit through the alimentary canal by determining the degree to which breast-fed infants' urine and fecal oligosaccharides resembled those of their mothers' milk. Oligosaccharide profiles of milk from 16 breast-feeding mothers were compared with profiles of stool and urine from their infants. Results were compared with endogenous oligosaccharide profiles obtained from the urine and feces of age-, parity-, and gender-matched formula-fed infants. In all cases, oligosaccharides were extracted, purified, reduced, and separated into acidic and neutral species; the latter were perbenzoylated and subjected to reversed-phase high-performance liquid chromatography. Structures were determined by mass spectrometry after debenzoylation. Among breast-fed infants, concentrations of oligosaccharides were higher in feces than in mothers' milk, and much higher in feces than in urine. Urinary and fecal oligosaccharides from breast-fed infants resembled those in their mothers' milk. Those from formula-fed infants did not resemble human milk oligosaccharides, were found at much lower concentrations, and probably resulted from remodeling of intestinal glycoconjugates or from intestinal bacteria. Most of the human milk oligosaccharides survived transit through the gut, and some were absorbed and then excreted into the urine intact, implying that inhibition of intestinal and urinary pathogens by human milk oligosaccharides is quite likely in breast-fed infants.
几种人乳寡糖在体外和动物模型中可抑制人类病原体。对于婴儿而言，这些寡糖若要提供针对肠道病原体的保护作用，就需要它们在通过消化道或被吸收并经尿液排泄的过程中耐受结构改变。我们通过测定母乳喂养婴儿尿液和粪便中的寡糖与母乳中寡糖的相似程度，来研究人乳寡糖在消化道转运过程中的去向。将16位母乳喂养母亲的母乳寡糖谱与她们婴儿的粪便和尿液寡糖谱进行了比较。结果与从年龄、胎次和性别匹配的配方奶喂养婴儿的尿液和粪便中获得的内源性寡糖谱进行了对比。在所有情况下，寡糖均被提取、纯化、还原，并分离为酸性和中性组分；后者经全苯甲酰化后进行反相高效液相色谱分析。脱苯甲酰化后通过质谱测定结构。在母乳喂养婴儿中，粪便中寡糖的浓度高于母乳，且粪便中的浓度远高于尿液。母乳喂养婴儿尿液和粪便中的寡糖与母乳中的相似。配方奶喂养婴儿的尿液和粪便寡糖与母乳寡糖不同，其浓度低得多，可能是肠道糖缀合物重塑或肠道细菌作用的结果。大多数人乳寡糖在通过肠道的过程中存活下来，一些被吸收后完整地排泄到尿液中，这意味着人乳寡糖很可能在母乳喂养婴儿中抑制肠道和泌尿系统病原体。
