No significant differences in weight gain or stool SCFA content were detected.

The production of SCFA increased with the level of supplied NT equivalents.

SCFA levels were significantly higher in portal vs. hepatic and peripheral blood.

No significant differences in stool SCFA content were detected between groups.

SCFA had no significant effect on serum insulin or c-peptide concentrations.

This was associated with an altered fecal SCFA and BA profile.

In addition, the data provide indirect evidence for utilization of SCFA for lipid synthesis.

The fall in FFA suggests that colonic SCFA have an effect on carbohydrate metabolism.

However, the mechanisms underlying SCFA regulation of T-cell differentiation and function remain to be investigated.

The ratios of SCFA formed differed depending on the microbial species involved in mucin cross-feeding.

Analytical data on faecal samples support the role of the colonic microbial population in SCFA production.

The data provide strong evidence that colonic SCFA are absorbed and metabolized in the human subject.

In all groups SCFA concentrations were highest in the proximal colon and decreased towards the rectum.

Increased melanoidins was found to result in significantly divergent gut microbiota profiles and supported sustained SCFA production.

The main SCFA are acetate, propionate and butyrate which have numerous documented effects promoting large bowel function.

Dietary stevia leave and stevioside decreased total concentration of SCFA and changed their profile in the ceca.