用户名: 密码: 验证码:
Relative fermentation of oligosaccharides from human milk and plants by gut microbes
详细信息    查看全文
文摘
Gut microbiota is important to human health. Specific dietary glycans promote favorable microbiota growth and inhibit pathobionts. Dietary glycans most relevant to adults and weaned infants are derived from plants or lactose; human milk oligosaccharides (HMOS) are most relevant to breastfed infants. Their efficacy in supporting bacterial growth is compared to determine their potential roles in the initiation and maintenance of colonization. Bioactivities of gluco-manno-oligosaccharides (GMOS), galacto-oligosaccharides (GOS), xylo-oligosaccharides (XOS), cellobiose (CBS), HMOS, and the most prominent individual HMOS, 2′-fucosyllactose (2′-FL) were contrasted. Two representative gut microbiota mutualists, Bifidobacteria longum ATCC15697 and Lactobacillus acidophilus NRRL B-4495, and two non-mutualists, Campylobacter jejuni S107 and Escherichia coli K12, were used to assess the in vitro prebiotic potential of these oligosaccharides. All oligosaccharides afforded growth of B. longum and L. acidophilus, with HMOS supporting the most robust growth, while none of these oligosaccharides afforded meaningful growth of non-mutualists. B. longum efficiently converted HMOS, GMOS, GOS, and XOS into organic acid fermentation products, and, to a lesser degree, L. acidophilus metabolized HMOS, GMOS, and GOS. Fermentation of these glycans by C. jejuni and E. coli was sparse. B. longum fermentation products inhibited C. jejuni and E. coli. Thus, HMOS most strongly promoted growth of the two mutualists, and both HMOS and GMOS were efficiently fermented by these mutualists into organic acids. This is consistent with a primary role of HMOS in guiding early colonization of the infant microbiota by mutualist symbionts, and of plant oligosaccharides, especially GMOS, in maintaining a favorable microbiota through adulthood.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700