PMID- 24325781
OWN - NLM
STAT- MEDLINE
DCOM- 20141201
LR  - 20220318
IS  - 1440-1746 (Electronic)
IS  - 0815-9319 (Linking)
VI  - 29
IP  - 5
DP  - 2014 May
TI  - Effects of dietary supplementation of glucosamine sulfate on intestinal 
      inflammation in a mouse model of experimental colitis.
PG  - 957-63
LID - 10.1111/jgh.12485 [doi]
AB  - 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-alpha (TNF-alpha), interleukin-1beta, 
      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-kappaB activation and related inflammatory 
      responses.
CI  - (c) 2013 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing 
      Asia Pty Ltd.
FAU - Bak, Youn-Kyung
AU  - Bak YK
AD  - Department of Food and Nutrition, Sookmyung Women's University, Seoul, Korea.
FAU - Lampe, Johanna W
AU  - Lampe JW
FAU - Sung, Mi-Kyung
AU  - Sung MK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - J Gastroenterol Hepatol
JT  - Journal of gastroenterology and hepatology
JID - 8607909
RN  - 0 (Acute-Phase Proteins)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipocalin-2)
RN  - 0 (Lipocalins)
RN  - 0 (NF-kappa B)
RN  - 0 (Occludin)
RN  - 0 (Oncogene Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Serum Amyloid P-Component)
RN  - 0 (Tjp1 protein, mouse)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Zonula Occludens-1 Protein)
RN  - 126469-30-5 (Lcn2 protein, mouse)
RN  - 9042-14-2 (Dextran Sulfate)
RN  - N08U5BOQ1K (Glucosamine)
SB  - IM
MH  - Acute-Phase Proteins/metabolism
MH  - Administration, Oral
MH  - Animals
MH  - Colitis/chemically induced/genetics/metabolism/*prevention & control
MH  - Colon/*metabolism
MH  - Dextran Sulfate
MH  - *Dietary Supplements
MH  - Disease Models, Animal
MH  - Gene Expression
MH  - Glucosamine/*administration & dosage
MH  - Inflammation Mediators/*metabolism
MH  - Interleukin-1beta/genetics/metabolism
MH  - Interleukin-8/blood
MH  - Lipocalin-2
MH  - Lipocalins/metabolism
MH  - Mice, Inbred C57BL
MH  - NF-kappa B/genetics/metabolism
MH  - Occludin/metabolism
MH  - Oncogene Proteins/metabolism
MH  - Precancerous Conditions
MH  - RNA, Messenger/metabolism
MH  - Serum Amyloid P-Component/metabolism
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
MH  - Zonula Occludens-1 Protein/metabolism
OTO - NOTNLM
OT  - colitis
OT  - colorectal cancer
OT  - glucosamine
OT  - inflammation
OT  - tight junction protein
EDAT- 2013/12/12 06:00
MHDA- 2014/12/15 06:00
CRDT- 2013/12/12 06:00
PHST- 2013/11/05 00:00 [accepted]
PHST- 2013/12/12 06:00 [entrez]
PHST- 2013/12/12 06:00 [pubmed]
PHST- 2014/12/15 06:00 [medline]
AID - 10.1111/jgh.12485 [doi]
PST - ppublish
SO  - J Gastroenterol Hepatol. 2014 May;29(5):957-63. doi: 10.1111/jgh.12485.