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We hypothesized that daily intake of nondigestible saccharides delays senescence onset through the improvement of intestinal microflora. Here, we raised senescence accelerated mice prone 8 (SAMP8) on the AIN93 diet (CONT), with sucrose being substituted for 5% of fructooligosaccharide (FOS) or 5% of glucomannan (GM), 15 mice per group. Ten SAMR1 were raised as reference of normal aging with control diet. Grading of senescence was conducted using the method developed by Hosokawa, and body weight, dietary intake, and drinking water intake were measured on alternate days. Following 38 weeks of these diets we evaluated learning and memory abilities using a passive avoidance apparatus and investigated effects on the intestinal microflora, measured oxidative stress markers, and inflammatory cytokines. Continuous intake of FOS and GM significantly enhanced learning and memory ability and decelerated senescence development when compared with the CONT group. Bifidobacterium levels were significantly increased in FOS and GM-fed mice. Urinary 8OHdG, 15-isoprostane, serum TNF-α, and IL-6 were also lower in FOS-fed mice, while IL-10 in FOS and GM groups was higher than in CONT group. These findings suggest that daily intake of nondigestible saccharides delays the onset of senescence via improvement of intestinal microflora.

Morus alba leaf extract (MLE), a strong inhibitor of sucrase, suppresses blood glucose elevation following sucrose ingestion. To investigate that sucrose inhibited from digestion using MLE is utilized through gut microbiota, [U-14 C]-sucrose solutions with or without MLE were administered orally to conventional and antibiotic-treated rats, and the excretion of 14 CO2 and H2 produced by gut microbiota was measured for 24 h. After an administration of [U-14 C]-sucrose to conventional rats, the unit excreted 14 CO2 peaked at 4 h, and the cumulative 14 CO2 excreted over 24 h was approximately 60% of the radioactivity administered. No H2 was excreted. Following an administration of [U-14 C]-sucrose and MLE in conventional rats, the unit excreted 14 CO2 peaked later, at 8 h, and was significantly lower (p,0.05). The cumulative 14 CO2 excreted over 24 h was equal in both groups, although there was a time lag of 2-3 h in rats given [U-14 C]-sucrose and MLE. The amount of H2 excreted by these rats peaked 8 h after administration. Following the administration of [U-14 C]-sucrose and MLE to antibiotic-treated rats, the unit excreted 14 CO2 peaked lower, and the cumulative 14 CO2 excretion over 24 h was approximately 40%. In this group, H2 was minimally excreted. H2 and 14 CO2 produced by gut microbiota were excreted simultaneously. In conclusion, sucrose inhibited from digestion using MLE was fermented spontaneously by gut microbiota and was not excreted into feces. In addition, it confirmed that H2 excretion could be used directly to indicate the degree of fermentation of nondigestible carbohydrates.

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