The fate of stable-isotope (13)C labelled and non-labelled inulin catabolism by the gut microbiota was assessed in a healthy rat model. Sprague-Dawley male rats were randomly assigned to diets containing either cellulose or inulin, and were fed these diets for 3 days. On day (d) 4, rats allocated to the inulin diet received (13)C-labelled inulin. The rats were then fed the respective non-labelled diets (cellulose or inulin) until sampling (d4, d5, d6, d7, d10 and d11). Post feeding of (13)C-labelled substrate, breath analysis showed that (13)C-inulin cleared from the host within a period of 36 hours. Faecal (13)C demonstrated the clearance of inulin from gut with a (13)C excess reaching maximum at 24 hours (d5) and then declining gradually. There were greater variations in caecal organic acid concentrations from d4 to d6, with higher concentrations of acetic, butyric and propionic acids observed in the rats fed inulin compared to those fed cellulose. Inulin influenced caecal microbial glycosidase activity, increased colon crypt depth, and decreased the faecal output and polysaccharide content compared to the cellulose diet. In summary, the presence of inulin in the diet positively influenced large bowel microbial fermentation.

This study investigated the impact of ACTAZIN™ green (2400 and 600 mg) and Livaux™ (2400 mg) gold kiwifruit supplements on faecal microbial composition and metabolites in healthy and functionally constipated (FC) participants. The participants were recruited into the healthy group (n 20; one of whom did not complete the study) and the FC group (n 9), each of whom consumed all the treatments and a placebo (isomalt) for 4 weeks in a randomised cross-over design interspersed with 2-week washout periods. Modification of faecal microbiota composition and metabolism was determined by 16S rRNA gene sequencing and GC, and colonic pH was calculated using SmartPill® wireless motility capsules. A total of thirty-two taxa were measured at greater than 1 % abundance in at least one sample, ten of which differed significantly between the baseline healthy and FC groups. Specifically, Bacteroidales and Roseburia spp. were significantly more abundant (P < 0·05) in the healthy group and taxa including Ruminococcaceae, Dorea spp. and Akkermansia spp. were significantly more abundant (P < 0·05) in the FC group. In the FC group, Faecalibacterium prausnitzii abundance significantly increased (P = 0·024) from 3·4 to 7·0 % following Livaux™ supplementation, with eight of the nine participants showing a net increase. Lower proportions of F. prausnitzii are often associated with gastrointestinal disorders. The discovery that Livaux™ supplementation increased F. prausnitzii abundance offers a potential strategy for improving gut microbiota composition, as F. prausnitzii is a butyrate producer and has also been shown to exert anti-inflammatory effects in many studies.

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We examined the effects of whole kiwifruit on gut microbiota using an in vitro batch model of gastric-ileal digestion and colonic fermentation. Faecal fermentations of gold and green kiwifruit, inulin and water (control) digests were performed for up to 48 h. As compared to the control, gold and green kiwifruit increased Bifidobacterium spp. by 0.9 and 0.8 log(10) cfu/ml, respectively (P < 0.001), and the Bacteroides-Prevotella-Porphyromonas group by 0.4 and 0.5 log(10) cfu/ml, respectively. Inulin only had a bifidogenic effect (+0.4 log(10) cfu/ml). This was accompanied with increases in microbial glycosidases, especially those with substrate specificities relating to the breakdown of kiwifruit oligosaccharides, and with increased generation of short chain fatty acids. The microbial metabolic activity was sustained for up to 48 h, which we attribute to the complexity of the carbohydrate substrate provided by whole kiwifruit. Kiwifruit fermenta supernatant was also separately shown to affect the in vitro proliferation of Bifidobacterium longum, and its adhesion to Caco-2 intestinal epithelial cells. Collectively, these data suggest that whole kiwifruit may modulate human gut microbial composition and metabolism to produce metabolites conducive to increased bifidobacteria-host association.