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Luminal fructose induces endoplasmic reticulum (ER) stress and the unfolded protein response (UPR)‐PERK pathway in perfused rat small intestine
Author(s) -
patel chirag r,
douard Veronique,
Monteiro Cheryl,
Ferraris Ronaldo
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1108.6
Subject(s) - unfolded protein response , atf6 , endoplasmic reticulum , fructose , atf4 , glucose regulated protein , activating transcription factor , medicine , chemistry , endocrinology , biology , biochemistry
Fructose consumption worldwide has increased markedly and is thought to induce in various organs ER stress which is also known to contribute to pathogenesis of inflammatory bowel diseases. Since the small intestine is exposed to high concentrations of luminal fructose, we investigated in vivo in perfused rat small intestine the effect of 50 mM fructose (control: 50 mM glucose) on the mucosal mRNA expression of various proteins known to be associated with ER stress and the unfolded protein response (UPR). After 5 h, the relative expression of specific members of the PERK (PKR‐like ER‐localized eIF2α kinase) UPR pathway, binding immunoglobulin protein (BiP), significantly increased by 100%, activation transcription factor‐4 (ATF‐4) by 40%, and CCAAT/‐enhancer‐binding protein homologous protein (CHOP) by 39%. Thus, fructose likely induces the PERK but not the inositol‐requiring enzyme 1 (IRE1) and ATF6 pathways of the UPR to intestinal ER stress. In contrast, renal and hepatic expression of BiP, ATF‐4 and CHOP were not affected by acute fructose perfusion. Thus, luminal fructose at physiological concentrations can induce ER stress and the PERK‐mediated UPR response int the rat small intestine (NSF 10S‐1121049).