The effects of plantain non starch polysaccharide upon the gut bacteria

The non-starch polysaccharide (NSP) components from apple, oat, broccoli and plantain were tested as growth substrates for representatives of the major groups of intestinal bacteria, none of which was able to fully utilise the NSPs for growth.  More bacteria were able to use the soluble plantain NSP...

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Bibliographic Details
Main Author: Backman, Ruth Valerie
Published: University of Aberdeen 2009
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Online Access:http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521158
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Summary:The non-starch polysaccharide (NSP) components from apple, oat, broccoli and plantain were tested as growth substrates for representatives of the major groups of intestinal bacteria, none of which was able to fully utilise the NSPs for growth.  More bacteria were able to use the soluble plantain NSP fraction for growth than any other NSP tested, with the <i>Bacteroides </i>group showing the strongest growth response.  <i>E. coli</i> strains isolated from healthy people and Inflammatory bowel disease (IBD) patients were all able to utilise the soluble plantain substrate to the same high extent. A wide range of commensal anaerobes were able to bind to the insoluble plantain NSP in a strain specific manner that was independent of the ability to utilize the soluble plantain NSP for growth, with <i>E. coli </i>binding in the highest numbers to the insoluble NSP. The effects of plantain NSP were monitored <i>in vivo</i>, and only the <i>Bacteroides </i>group increased significantly after soluble plantain supplementation.  <i>E. coli </i>populations were volunteer-specific and unaltered after plantain supplementation. <i>Bacteroides </i>and <i>E. coli</i> were the two main groups affected by plantain NSP after the <i>in vitro </i>work, both of which have been implicated in IBD.  Binding to, and growth on plantain may therefore selectively alter the composition of the gut microbiota in patients.  Despite the stimulation of <i>E. coli</i> growth, addition of plantain to the diet may help to prevent colonization of the gut wall by providing this alternative binding substrate.