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Member
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Join Date: Aug 2006
Location: Arkansas
Posts: 239
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Member
Join Date: Aug 2006
Location: Arkansas
Posts: 239
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Quote:
Originally Posted by mle_ii
Where did you read this about Zonulin being made by every person who eats wheat? I'd like to read the chemistry/biology behind this mechanism. I have some guesses, but I'm curious about the findings.
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There are many references to "increased" Zonulin levels in those with CD, DMT1 and other autoimmune diseases.
Danna Korn on says
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Dr. Fasano's research has shown that zonulin levels increase in EVERYONE who eats wheat -- not just celiacs.
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http://www.clanthompson.com/news_arc...&category_id=4
There is a good article on Zonulin in the current issue of the GIG Newsletter. To read the complete article you will have to join GIG or find a member and borrow the magazine.
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Experiments showed that gluten stimulated the relaese of zonulin in both celiacs and non-celiacs.
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Found this on Pubmed. Too bad there is not a currently available test for "too much" zonulin.
http://www.ncbi.nlm.nih.gov/entrez/q...play&DB=pubmed
Quote:
Scand J Gastroenterol. 2006 Apr;41(4):408-19.
Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines.
Drago S, El Asmar R, Di Pierro M, Grazia Clemente M, Tripathi A, Sapone A, Thakar M, Iacono G, Carroccio A, D'Agate C, Not T, Zampini L, Catassi C, Fasano A.
Mucosal Biology Research Center, Center for Celiac Research and Division of Pediatric Gastroenterology and Nutrition, University of Maryland, School of Medicine, Baltimore, MD 21201, USA.
OBJECTIVE: Little is known about the interaction of gliadin with intestinal epithelial cells and the mechanism(s) through which gliadin crosses the intestinal epithelial barrier. We investigated whether gliadin has any immediate effect on zonulin release and signaling. MATERIAL AND METHODS: Both ex vivo human small intestines and intestinal cell monolayers were exposed to gliadin, and zonulin release and changes in paracellular permeability were monitored in the presence and absence of zonulin antagonism. Zonulin binding, cytoskeletal rearrangement, and zonula occludens-1 (ZO-1) redistribution were evaluated by immunofluorescence microscopy. Tight junction occludin and ZO-1 gene expression was evaluated by real-time polymerase chain reaction (PCR). RESULTS: When exposed to gliadin, zonulin receptor-positive IEC6 and Caco2 cells released zonulin in the cell medium with subsequent zonulin binding to the cell surface, rearrangement of the cell cytoskeleton, loss of occludin-ZO1 protein-protein interaction, and increased monolayer permeability. Pretreatment with the zonulin antagonist FZI/0 blocked these changes without affecting zonulin release. When exposed to luminal gliadin, intestinal biopsies from celiac patients in remission expressed a sustained luminal zonulin release and increase in intestinal permeability that was blocked by FZI/0 pretreatment. Conversely, biopsies from non-celiac patients demonstrated a limited, transient zonulin release which was paralleled by an increase in intestinal permeability that never reached the level of permeability seen in celiac disease (CD) tissues. Chronic gliadin exposure caused down-regulation of both ZO-1 and occludin gene expression. CONCLUSIONS: Based on our results, we concluded that gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules.
PMID: 16635908 [PubMed - indexed for MEDLINE]
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Anne
Last edited by annelb; 09-12-2006 at 09:10 PM.
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09-12-2006, 09:07 PM
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