title: Decreased Expression of Enterocyte Nutrient Assimilation Genes and Proteins in the Small Intestine of Cystic Fibrosis Mouse.
abstract: OBJECTIVE
  Cystic fibrosis (CF) has major effects on the intestinal tract with potential consequences on nutrition, but these are not fully understood. I investigated the possibility of altered enterocyte maturation in CF, as suggested by decreased enterocyte nutrient assimilation gene expression in published transcriptome analysis of the small intestine of CF mouse.
  
  
  METHODS
  In CF and wild-type (WT) mice, enterocyte gene/protein expression was analyzed by quantitative realtime polymerase chain reaction (qRT-PCR), enzyme histochemistry, immunohistochemistry, and Western blot. One group of mice was maintained on a control liquid diet; to manipulate the gut microbiota, a second group was treated with oral antibiotics; to improve hydration of the gut lumen, a third group was given a laxative drinking solution.
  
  
  RESULTS
  On the control diet in the CF intestine, there were decreased levels (67%-85% reduction of WT levels) of enterocyte genes/proteins. Antibiotics did not normalize the expression of enterocyte markers in the CF mouse. In contrast, the laxative treatment of CF mice significantly increased expression to near WT levels.
  
  
  CONCLUSIONS
  These studies suggest that the environment of the CF intestinal lumen plays a role in reduced maturation of enterocytes. Because changing the gut lumen environment can affect enterocyte maturation, this is not a cell-autonomous effect of loss of CF transmembrane conductance regulator.
authors.affiliation: Anatomy and Cell Biology, University of Kansas School of Medicine, Kansas City, KS.
authors.forename: Robert C
authors.initials: RC
authors.lastname: De Lisle
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D002454:Cell Differentiation / Q000187:drug effects; D003131:Combined Modality Therapy; D003550:Cystic Fibrosis / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology / Q000628:therapy; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000235:genetics; D015536:Down-Regulation / Q000187:drug effects; D064806:Dysbiosis / Q000209:etiology / Q000517:prevention & control; D004734:Energy Metabolism / Q000187:drug effects; D020895:Enterocytes / Q000187:drug effects / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D005260:Female; D005440:Fluid Therapy; D000069196:Gastrointestinal Microbiome / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D007421:Intestine, Small / Q000187:drug effects / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D054368:Laxatives / Q000627:therapeutic use; D008297:Male; D018345:Mice, Knockout
chemical_list: D000900:Anti-Bacterial Agents; D054368:Laxatives; D019005:Cystic Fibrosis Transmembrane Conductance Regulator