Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3291872 | Gastroenterology | 2016 | 26 Pages |
Abstract
Mice with defects in intestinal epithelial permeability develop more severe steatohepatitis after a HFCD than control mice, and colon tissues from patients with NAFLD have lower levels of JAM-A and higher levels of inflammation than subjects without NAFLD. These findings indicate that intestinal epithelial barrier function and microbial dysbiosis contribute to the development of NASH. Restoration of intestinal barrier integrity and manipulation of gut microbiota might be developed as therapeutic strategies for patients with NASH.
Keywords
rRNAHSCALTNAFLαSMATLRCRNFITCJAM-AJunctional adhesion molecule ALPSNAFLDRibosomal RNAα smooth muscle actinASTAspartate aminotransferaseAlanine aminotransferaseTight junctionnonalcoholic steatohepatitisBacterial translocationinterleukinNonalcoholic fatty liver diseaseToll-like receptorHepatic stellate cellMetabolic syndromeClinical Research NetworkOccludinfluorescein isothiocyanatelipopolysaccharideMETSNash polymerase chain reactionPCRNonalcoholic fatty liverClaudin-4
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Authors
Khalidur Rahman, Chirayu Desai, Smita S. Iyer, Natalie E. Thorn, Pradeep Kumar, Yunshan Liu, Tekla Smith, Andrew S. Neish, Hongliang Li, Shiyun Tan, Pengbo Wu, Xiaoxiong Liu, Yuanjie Yu, Alton B. Farris, Asma Nusrat, Charles A. Parkos, Frank A. Anania,