Colonic Hydrogen Generated from Fructan Diffuses into the Abdominal Cavity and Reduces Adipose mRNA Abundance of Cytokines in Rats.

Hydrogen (H₂) protects against inflammation-induced oxidative stress. Nondigestible saccharides (NDSs) enhance colonic H₂ production. We examined whether colonic H₂ transfers to tissues in the abdominal cavity and whether it affects expression of proinflammatory cytokines. In Expts. 1 and 2, rats were fed diets containing fructooligosaccharides [FOSs; 25 (Expt. 1) and 50 g/kg (Expts. 1 and 2)] for 7 and 14 d, respectively. The no-FOS diet was used as the control diet. At the end of the experiment, H₂ excretion and the portal H₂ concentration were significantly greater in the FOS group than in the control group. In the FOS group, the arterial H2 concentration was no more than 1.5% of the portal H2 concentration (P = 0.03). The H₂ concentration in abdominal cavity tissues, especially adipose tissue, in the FOS group was 5.6- to 43-fold of that in the control group (P < 0.05). The H2 content in the abdominal cavity in the FOS group was 11-fold of that in the control group (P < 0.05). In Expt. 3, rats were fed a high-fat diet containing FOS and inulin (50 g/kg) for 28 d. The area under the curve for H₂ excretion between 0 and 28 d and portal and adipose H₂ concentrations were significantly higher in the FOS and inulin groups than in the high-fat control group. Adipose mRNA abundance of nuclear factor kappa-light-chainenhancer of activated B cells 1 was lower in the FOS group than in the control group (P = 0.02) and those of interleukin-6 and chemokine (C-C motif) ligand 2 tended to be lower (P < 0.11). Colonic H₂ generated from NDS diffuses to the abdominal cavity before transferring to abdominal tissues. Reduced cytokine expression by FOS feeding might be dependent on increased colonic H₂. Colonic H₂ may have important implications in the suppressive effect on metabolic syndrome via oxidative stress. [ABSTRACT FROM AUTHOR]