Lactulose Boosts Gut Hydrogen to Fight Colon Inflammation in Mice

Authors
Journal
Digestive Diseases and Sciences
Year
DOI
10.1007/s10620-013-2563-7
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Ulcerative Colitis
Body System
Digestive System

TL;DR

Lactulose, a type of sugar, can help prevent and reduce inflammation in a mouse model of colon inflammation by increasing the production of hydrogen gas in the body.

Key Finding

Lactulose reduced colon inflammation and oxidative stress in mice with induced colitis, but only when gut bacteria were present to ferment it and produce hydrogen gas.

Summary

This mouse study tested whether lactulose, a type of sugar that gut bacteria ferment to produce hydrogen gas, could reduce inflammation in the colon. Mice given lactulose showed less colon damage, lower levels of inflammatory markers, and reduced oxidative stress (cellular damage from unstable molecules) compared to mice with induced colitis. When antibiotics were given alongside lactulose, the protective effect largely disappeared, suggesting that the beneficial bacteria in the gut are essential for this process to work.

Practical Takeaway

This is an early-stage animal study suggesting that hydrogen production from lactulose fermentation may help protect the colon from inflammation. However, results in mice do not automatically translate to humans, and this study does not demonstrate that lactulose or hydrogen water would benefit people with ulcerative colitis or other digestive conditions. Human clinical trials would be needed to determine if this approach has real therapeutic value.

Abstract

Background: Molecular hydrogen (H2) is a potent antioxidant and able to protect organs from oxidative stress injuries. Orally administered lactulose, a potent H2 inducer, is digested by colon microflora and significantly increases H2 production, indicating its potential anti-inflammatory action. Objective: To evaluate the anti-inflammatory effects of lactulose on dextran sodium sulfate (DSS)-induced colitis in mice. Methods: Mice were randomly assigned into seven groups, receiving regular distilled water, H2-rich saline (peritoneal injection), DSS, oral lactulose (0.1, 0.15, 0.2 ml/10 g, respectively), and lactulose (0.2 ml/10 g) + oral antibiotics. The mouse model of human ulcerative colitis was established by supplying mice with water containing DSS. The H2 breath test was used to determine the exhaled H2 concentration. Body weight, colitis score, colon length, pathological features and tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), maleic dialdehyde (MDA) and marrow peroxidase (MPO) levels in colon lesions were evaluated. Results: After 7 days, DSS-induced loss of body weight, increase of colitis score, shortening of colon length, pathological changes and elevated levels of TNF-α, IL-1β, MDA, and MPO in colon lesions, were significantly suppressed by oral lactulose administration and intraperitoneally injected H2-rich saline. Ingestion of antibiotics significantly compromised the anti-inflammatory effects of lactulose. The H2 breath test showed that lactulose administration significantly induced hydrogen production and that antibiotics administration could inhibit H2 production. Conclusion: Lactulose can prevent the development of DSS-induced colitis and alleviate oxidative stress in the colon, as measured by MDA and MPO, probably by increasing endogenous H2 production.