Accumulating evidence suggests an association between gut microbiota and the development of obesity, raising the possibility of probiotic administration as a therapeutic approach. Bifidobacterium breve B-3 was found to exhibit an anti-obesity effect on high-fat diet-induced obesity mice. In the present study, a randomised, double-blind, placebo-controlled trial was conducted to evaluate the effect of the consumption of B. breve B-3 on body compositions and blood parameters in adults with a tendency for obesity. After a 4-week run-in period, the participants were randomised to receive either placebo or a B-3 capsule (approximately 5 × 1010 colony-forming units of B-3/d) daily for 12 weeks. A significantly lowered fat mass was observed in the B-3 group compared with the placebo group at week 12. Improvements were observed for some blood parameters related to liver functions and inflammation, such as γ-glutamyltranspeptidase and high-sensitivity C-reactive protein. Significant correlations were found between the changed values of some blood parameters and the changed fat mass in the B-3 group. These results suggest the beneficial potential of B. breve B-3 in improving metabolic disorders.

The present study reports data on absorption of orally administered glutathione (GSH) in rat jejunum and in other organs, and the possible role of specific transport systems of GSH and γ-glutamyltranspeptidase (EC 2.3.2.1; γ-GT) activity. GSH levels were measured simultaneously in various organs after oral GSH administration to untreated rats and rats treated with L-buthionine sulfoximine (BSO) or acivicin (AT125). BSO selectively inhibits GSH intracellular synthesis and AT125 is a specific inhibitor of γ-GT activity. GSH levels were also measured after oral administration of an equivalent amount of the constituent amino acids of GSH to untreated and BSO-treated rats. Significant increases in GSH levels were found in jejunum, lung, heart, liver and brain after oral GSH administration to untreated rats. GSH increases were also obtained in all organs, except liver, when GSH was administered to rats previously GHS-depleted by treatment with BSO. The analysis of all results allowed us to distinguish between the increase in GSH intracellular levels due to intact GSH uptake by specific transporters, and that due to GSH degradation by γ-GT activity and subsequent absorption of degradation products with intracellular resynthesis of GSH; both these mechanisms seemed to be involved in increasing GSH content in heart after oral GSH administration. Jejunum, lung and brain took up GSH mostly intact, by specific transport systems, while in liver GSH uptake occurred only by its breakdown by γ-GT activity followed by intracellular resynthesis.