Sialic acid feeding aged rats rejuvenates stimulated salivation and colon enteric neuron chemotypes.

Old age is linked to numerous changes of body functions such as salivation, gastrointestinal motility, and permeability all linked to central and enteric nervous system decline. Thus, gut motility and barrier functions suffer. Sialic acid plays a key role in the nervous system at large and for many receptor functions specifically. Decreased sialylation in the elderly suggests an endogenous sialic acid deficit. We used a rat model of aging, to ask whether sialic acid feeding would affect (i) stimulated salivation, (ii) gut functions, and (iii) sialic acid levels and neuronal markers in brain and gut. We observed reduced levels of pilocarpine-stimulated salivation in old versus young rats and restored this function by sialic acid feeding. Brain ganglioside bound sialic acid levels were found lower in aged versus young rats, and sialic acid feeding partly restored the levels. The hypothalamic expression of cholinergic and panneuronal markers was reduced in aged rats. The expression of the nitrergic marker nNOS was increased upon sialic acid feeding in aged rats. Neither fecal output nor gut permeability was different between young and aged rats studied here, and sialic acid feeding did not alter these parameters. However, the colonic expression of specific nervous system markers nNOS and Uchl1 and the key enzyme for sialic acid synthesis GNE were differentially affected in young and aged rats by sialic acid feeding indicating that regulatory mechanisms change with age. Investigation of sialic acid supplementation as a functional nutrient in the elderly may help those who suffer from disorders of reduced salivation. Further research is needed to understand the differential effects of sialic acid feeding in young and aged rats.

Chicory increases acetate turnover, but not propionate and butyrate peripheral turnovers in rats.

Chicory roots are rich in inulin that is degraded into SCFA in the caecum and colon. Whole-body SCFA metabolism was investigated in rats during food deprivation and postprandial states. After 22 h of food deprivation, sixteen rats received an IV injection of radioactive 14C-labelled SCFA. The volume of distribution and the fractional clearance rate of SCFA were 0.25-0.27 litres/kg and 5.4-5.9 %/min, respectively. The half-life in the first extracellular rapidly decaying compartment was between 0.9 and 1.4 min. After 22 h of food deprivation, another seventeen rats received a primed continuous IV infusion of 13C-labelled SCFA for 2 h. Isotope enrichment (13C) of SCFA was determined in peripheral arterial blood by MS. Peripheral acetate, propionate and butyrate turnover rates were 29, 4 and 0.3 micromol/kg per min respectively. Following 4 weeks of treatment with chicory root or control diets, eighteen fed rats received a primed continuous IV infusion of 13C-labelled SCFA for 2 h. Intestinal degradation of dietary chicory lowered caecal pH, enhanced caecal and colonic weights, caecal SCFA concentrations and breath H2. The diet with chicory supplementation enhanced peripheral acetate turnover by 25 % (P = 0.017) concomitant with an increase in plasma acetate concentration. There were no changes in propionate or butyrate turnovers. In conclusion, by setting up a multi-tracer approach to simultaneously assess the turnovers of acetate, propionate and butyrate it was demonstrated that a chronic chicory-rich diet significantly increases peripheral acetate turnover but not that of propionate or butyrate in rats.

Fructooligosaccharides and fiber partially prevent the alterations in fecal microbiota and short-chain fatty acid concentrations caused by standard enteral formula in healthy humans.

The intestinal microbiota are important during enteral tube feeding because they exert colonization resistance and produce SCFAs. However, the effect of the enteral formula composition on major bacterial groups of the microbiota has not been clearly defined. The aim of this study was to investigate the effect of enteral formulas with and without prebiotic fructooligosaccharides (FOS) and fiber on the fecal microbiota and SCFAs. Healthy subjects (n = 10; 4 men, 6 women) consumed both a standard enteral formula and one containing FOS (5.1 g/L) and fiber (8.9 g/L) as a sole source of nutrition for 14 d in a randomized, double-blind, crossover trial with a 6-wk washout phase. Fecal samples were collected at the start and end of each formula phase, and were analyzed for major bacterial groups and SCFA concentrations using fluorescent in situ hybridization and GLC, respectively. Although there were reductions in total fecal bacteria due to both formula treatments, concentrations were higher after the FOS/fiber formula period compared with the standard formula period (11.2 +/- 0.2 vs. 11.0 +/- 0.2 log(10) cells/g, P = 0.005). The FOS/fiber formula increased bifidobacteria (P = 0.004) and reduced clostridia (P = 0.006). Compared with the standard formula, the FOS/fiber formula resulted in higher concentrations of total SCFA (332.4 +/- 133.8 vs. 220.1 +/- 124.5 micromol/g, P = 0.022), acetate (219.6 +/- 96.3 vs. 136.8 +/- 74.5 micromol/g, P = 0.034) and propionate (58.4 +/- 37.4 vs. 35.6 +/- 25.5 micromol/g, P = 0.02). This study demonstrates that standard enteral formula leads to adverse alterations to the fecal microbiota and SCFA concentrations in healthy subjects, and these alterations are partially prevented by fortification of the formula with FOS and fiber.