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Therefore, the effect of FOS on IgA induction varies widely among individuals.
Also it is not known if any of the above mentioned mechanisms or others are responsible for the effect of FOS on gut permeability.
Thus, the individual difference in the effect of FOS on faecal IgA concentration could be due to the individual differences in their gut microbiota and/or metabolites.
Some authors already cited a positive effect of FOS on the suppression of osmotic diarrhoea induced by maltitol but neither precise information nor possible mechanism was provided.
A statistically significant effect of FOS on the activity of β-glucosidase was recorded only in the case of diets with PTE preparation.
Taken together with the data on microbiota composition described above (Fig. 2), these results indicate that interindividual differences are too large for population analyses such as PCA to extract significant parameters contributing to the FOS-induced differences, and that intraindividual analysis could instead reveal the mechanisms for the effect of FOS on IgA production in humans.
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Energy-corrected milk (ECM) was affected by the interaction between starch and FO, with a positive effect of FO on the LS diet.
However, changes linked to FO-induced MFD (e.g., decreases in 18 0 and increases in total trans-18 1) trans-18 1ger in caprine rumen fluid, wereh may explain their unexpected strongerbinity (although less marked than in bovine) to the negative effecaprineO on milk fat content.
We evaluated the effect of FO on the occurrence of AKI in the entire cohort.
We used a logistic regression model to evaluate the effect of FO on the incidence of AKI.
Our results suggest that MCTs or MUFAs in the background diet might promote the beneficial effects of FO on CVDs.
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