Document Detail


Atherogenic diets exacerbate colitis in mice deficient in glutathione peroxidase.
MedLine Citation:
PMID:  20848490     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: The proinflammatory effect of high-fat diet has been observed beyond the cardiovascular system, but there is little evidence to support its role in triggering inflammatory bowel disease. GPx1/2-double-knockout (DKO) mice deficient in 2 intracellular glutathione peroxidases, GPx1 and GPx2, on a C57BL/6 (B6) background, have mild ileocolitis on a conventional chow.
METHODS: We fed B6 DKO mice 2 atherogenic diets to test the dietary effect on atherosclerosis and ileocolitis. Both atherogenic diets have high cholesterol-the Chol+/CA diet has cholic acid (CA), and the Chol+ diet has no CA.
RESULTS: The Chol+/CA diet induced severe colitis, but not ileitis, in the DKO mice compared with the Chol+ and the Chol- control diet. On the Chol+/CA diet, the wild-type (WT) mice had levels of aortic lesions and hypercholesterolemia similar to those of DKO mice but had no intestinal pathology. The diet-associated inflammatory responses in the DKO mice included increased colonic proinflammatory serum amyloid A3 expression, plasma lipopolysaccharide, and TNF-α levels. The Chol+/CA diet lowered the expression of the unfolded protein response genes ATF6, CHOP, unspliced Xbp(U) , and Grp78/Bip, in WT and DKO mice compared with mice on the Chol- diet.
CONCLUSIONS: We concluded that a cholesterol diet weakens the colon unfolded protein response, which can aggravate spontaneous colitis, leading to gut barrier breakdown. GPx has no impact on atherosclerosis without ultrahypercholesterolemia.
Authors:
Qiang Gao; R Steven Esworthy; Byung-Wook Kim; Timothy W Synold; David D Smith; Fong-Fong Chu
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Inflammatory bowel diseases     Volume:  16     ISSN:  1536-4844     ISO Abbreviation:  Inflamm. Bowel Dis.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-24     Completed Date:  2011-03-31     Revised Date:  2011-12-21    
Medline Journal Info:
Nlm Unique ID:  9508162     Medline TA:  Inflamm Bowel Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2043-54     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Crohn's & Colitis Foundation of America, Inc.
Affiliation:
Department of Radiation Biology, Beckman Research Institute of City of Hope, Duarte, California, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Atherosclerosis / etiology*,  pathology*
Blotting, Western
Cholesterol / metabolism
Colitis / etiology*,  pathology
Crohn Disease / etiology,  pathology
Deoxycholic Acid / metabolism
Diet, Atherogenic*
Fatty Liver / etiology,  pathology
Feces / chemistry
Female
Gas Chromatography-Mass Spectrometry
Glutathione Peroxidase / physiology*
Inflammation / etiology,  pathology
Inflammation Mediators / metabolism
Lipopolysaccharides / metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
RNA, Messenger / genetics
Reverse Transcriptase Polymerase Chain Reaction
Survival Rate
Tumor Necrosis Factor-alpha / metabolism
Grant Support
ID/Acronym/Agency:
R01 CA114569-05/CA/NCI NIH HHS; R01CA114569/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Inflammation Mediators; 0/Lipopolysaccharides; 0/RNA, Messenger; 0/Tumor Necrosis Factor-alpha; 57-88-5/Cholesterol; 83-44-3/Deoxycholic Acid; EC 1.11.1.-/Gpx2 protein, mouse; EC 1.11.1.-/glutathione peroxidase GPX1; EC 1.11.1.9/Glutathione Peroxidase

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