title: Lectins can reverse the distal intestinal atrophy associated with elemental diets in mice.
abstract: BACKGROUND
  Elemental diets cause intestinal atrophy and reduced intestinal integrity, which can lead to significant increases in intestinal permeability and bacterial translocation. Recently, several lectins have been shown to have trophic effects on the intestine.
  
  
  OBJECTIVE
  We examined the effects of concanavalin-A and phytohaemagglutinin on cell proliferation and crypt fission throughout the intestine of mice fed on elemental diets.
  
  
  METHODS
  Mice were randomized to chow fed, elemental diet, elemental diet plus concanavalin-A and elemental diet plus phytohaemagglutinin groups. Cell proliferation and crypt fission were estimated in microdissected crypts. Plasma gastrin and enteroglucagon levels were measured by radioimmunoassay.
  
  
  RESULTS
  Elemental diet feeding significantly decreased cell proliferation and crypt fission of the middle and distal small intestine and throughout the colon. Phytohaemagglutinin significantly increased the weight of the intestine, but concanavalin-A had little effect. Cell proliferation in the small intestine was significantly increased by both lectins. However, in the stomach and colon, only phytohaemagglutinin increased proliferation. Crypt fission in the colon was dramatically increased by phytohaemagglutinin. Phytohaemagglutinin increased the plasma gastrin level, but not the enteroglucagon level.
  
  
  CONCLUSIONS
  Lectins have significant trophic effects on the small intestine and colon of mice fed elemental diets, and these actions vary between different sites in the gastrointestinal tract.
authors.affiliation: Department of Histopathology, Imperial College School of Medicine, Hammersmith Hospital, London, UK.
authors.forename: M
authors.initials: M
authors.lastname: Sasaki
authors.forename: A J
authors.initials: AJ
authors.lastname: Fitzgerald
authors.forename: G
authors.initials: G
authors.lastname: Grant
authors.forename: M A
authors.initials: MA
authors.lastname: Ghatei
authors.forename: N A
authors.initials: NA
authors.lastname: Wright
authors.forename: R A
authors.initials: RA
authors.lastname: Goodlad
mesh_terms: D000818:Animals; D001284:Atrophy / Q000139:chemically induced* / Q000188:drug therapy / Q000473:pathology*; D002455:Cell Division / Q000187:drug effects; D003106:Colon / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D003208:Concanavalin A / Q000494:pharmacology; D005526:Food, Formulated / Q000009:adverse effects*; D005753:Gastric Mucosa / Q000378:metabolism; D005755:Gastrins / Q000097:blood; D007421:Intestine, Small / Q000187:drug effects* / Q000473:pathology* / Q000503:physiopathology; D037102:Lectins / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D008677:Metaphase / Q000187:drug effects; D051379:Mice; D009929:Organ Size / Q000187:drug effects; D027805:Phaseolus; D010835:Phytohemagglutinins / Q000494:pharmacology; D037121:Plant Lectins; D011863:Radioimmunoassay; D011897:Random Allocation; D013270:Stomach / Q000187:drug effects; D015430:Weight Gain / Q000187:drug effects
chemical_list: D005755:Gastrins; D037102:Lectins; D010835:Phytohemagglutinins; D037121:Plant Lectins; D003208:Concanavalin A