Fiber Supplements Create Hydrogen in Gut That Reduces Belly Fat Inflammation

Authors
Journal
The Journal of Nutrition
Year
DOI
10.3945/jn.113.183004
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
Japan
Health Condition
Metabolic Syndrome
Body System
Digestive

TL;DR

Eating certain sugars that can't be digested (like fructooligosaccharides) can increase hydrogen levels in the body, which may help reduce inflammation and stress-related damage in rats.

Key Finding

Hydrogen gas produced in the colon from dietary fiber diffuses into abdominal tissues—particularly fat tissue—where it accumulates at significantly higher levels than in the bloodstream, and this accumulation is associated with reduced expression of inflammatory markers.

Summary

Researchers fed rats a diet containing fructooligosaccharides (a type of fiber that humans cannot digest) and measured how hydrogen gas produced in the colon spreads through the body. They found that hydrogen accumulated in abdominal tissues, especially fat tissue, at levels 5 to 43 times higher than in rats eating a regular diet. In rats on a high-fat diet with added fiber, markers of inflammation in fat tissue were reduced, suggesting the hydrogen may have anti-inflammatory effects.

Practical Takeaway

This rat study suggests that certain dietary fibers (fructooligosaccharides and inulin) may increase hydrogen production in the colon, which could potentially reduce inflammation in fat tissue. However, this is early animal research; human studies would be needed to determine whether eating these fibers produces similar effects in people or whether it translates to meaningful health benefits.

Abstract

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-chain-enhancer 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.