Effects of dietary supplementation of glucosamine sulfate on intestinal inflammation in a mouse model of experimental colitis.

Abstract

BACKGROUND AND AIM:

Epidemiological evidences suggested an inverse association between the use of glucosamine supplements and colorectal cancer (CRC) risk. In this study, the efficacy of glucosamine to attenuate dextran sodium sulfate (DSS)-induced colitis, a precancerous condition for CRC, was evaluated.

METHODS:

C57BL/6 mice were separated into three groups receiving glucosamine sulfate at concentrations of 0, 0.05, and 0.10% (w/w) of AIN-93G diet, respectively for 4 weeks. Colitis was induced by supplying two cycles (5 days per cycle) of 2% DSS in the animals' drinking water.

RESULTS:

Glucosamine supplementation at the level of 0.10% of the diet (w/w) reduced colitis-associated symptoms as measured by disease activity index (DAI). Tumor necrosis factor-α (TNF-α), interleukin-1β, and nuclear factor-kappa B mRNA expression in the colonic mucosa was significantly lower in animals fed 0.10% glucosamine compared with those of the control group. Expression of the tight junction proteins ZO-1 and occludin was significantly higher in the 0.10% glucosamine-supplemented group compared with the other groups. Also, colonic protein expression of lipocalin 2, and serum concentrations of interleukin-8 and amyloid P component (SAP) were significantly reduced in the 0.10% glucosamine-supplemented group compared with the control group.

CONCLUSION:

These results suggest that glucosamine attenuates the colitis disease activity by suppressing NF-κB activation and related inflammatory responses.

• Authors: Youn-Kyung Bak, Johanna W Lampe, Mi-Kyung Sung
• Journal: Journal of gastroenterology and hepatology (J Gastroenterol Hepatol) Vol. 29 Issue 5 Pg. 957-63 (May 2014) ISSN: 1440-1746 [Electronic] Australia
• PMID: 24325781 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2013 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing Asia Pty Ltd.

Chemical References

• Acute-Phase Proteins
• Inflammation Mediators
• Interleukin-1beta
• Interleukin-8
• Lipocalin-2
• Lipocalins
• NF-kappa B
• Occludin
• Oncogene Proteins
• RNA, Messenger
• Serum Amyloid P-Component
• Tjp1 protein, mouse
• Tumor Necrosis Factor-alpha
• Zonula Occludens-1 Protein
• Lcn2 protein, mouse
• Dextran Sulfate
• Glucosamine

Topics

• Acute-Phase Proteins (metabolism)
• Administration, Oral
• Animals
• Colitis (chemically induced, genetics, metabolism, prevention & control)
• Colon (metabolism)
• Dextran Sulfate
• Dietary Supplements
• Disease Models, Animal
• Gene Expression
• Glucosamine (administration & dosage)
• Inflammation Mediators (metabolism)
• Interleukin-1beta (genetics, metabolism)
• Interleukin-8 (blood)
• Lipocalin-2
• Lipocalins (metabolism)
• Mice, Inbred C57BL
• NF-kappa B (genetics, metabolism)
• Occludin (metabolism)
• Oncogene Proteins (metabolism)
• Precancerous Conditions
• RNA, Messenger (metabolism)
• Serum Amyloid P-Component (metabolism)
• Tumor Necrosis Factor-alpha (genetics, metabolism)
• Zonula Occludens-1 Protein (metabolism)