title: Effects of dietary supplementation of glucosamine sulfate on intestinal inflammation in a mouse model of experimental colitis.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  These results suggest that glucosamine attenuates the colitis disease activity by suppressing NF-κB activation and related inflammatory responses.
authors: Department of Food and Nutrition, Sookmyung Women's University, Seoul, Korea.
authors: Youn-Kyung
authors: YK
authors: Bak
authors: Johanna W
authors: JW
authors: Lampe
authors: Mi-Kyung
authors: MK
authors: Sung
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism; D000284:Administration, Oral; D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D003106:Colon / Q000378:metabolism*; D016264:Dextran Sulfate; D019587:Dietary Supplements; D004195:Disease Models, Animal; D015870:Gene Expression; D005944:Glucosamine / Q000008:administration & dosage*; D018836:Inflammation Mediators / Q000378:metabolism*; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D016209:Interleukin-8 / Q000097:blood; D000071068:Lipocalin-2; D054834:Lipocalins / Q000378:metabolism; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D062793:Occludin / Q000378:metabolism; D015513:Oncogene Proteins / Q000378:metabolism; D011230:Precancerous Conditions; D012333:RNA, Messenger / Q000378:metabolism; D000683:Serum Amyloid P-Component / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D062826:Zonula Occludens-1 Protein / Q000378:metabolism
chemical_list: D000209:Acute-Phase Proteins; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D016209:Interleukin-8; D000071068:Lipocalin-2; D054834:Lipocalins; D016328:NF-kappa B; D062793:Occludin; D015513:Oncogene Proteins; D012333:RNA, Messenger; D000683:Serum Amyloid P-Component; C569043:Tjp1 protein, mouse; D014409:Tumor Necrosis Factor-alpha; D062826:Zonula Occludens-1 Protein; C071332:Lcn2 protein, mouse; D016264:Dextran Sulfate; D005944:Glucosamine
keywords: colitis; colorectal cancer; glucosamine; inflammation; tight junction protein