title: Naturally occurring glycoalkaloids in potatoes aggravate intestinal inflammation in two mouse models of inflammatory bowel disease.
abstract: BACKGROUND
  Inflammatory bowel disease (IBD) may be initiated following disruption of the intestinal epithelial barrier. This disruption, in turn, permits luminal antigens unfettered access to the mucosal immune system and leads to an uncontrolled inflammatory response. Glycoalkaloids, which are found in potatoes, disrupt cholesterol-containing membranes such as those of the intestinal epithelium. Glycoalkaloid ingestion through potatoes may play a role in the initiation and/or perpetuation of IBD.
  
  
  OBJECTIVE
  To determine if commercial and high glycoalkaloids containing fried potato skins aggravate intestinal inflammation using two different animal models of IBD.
  
  
  METHODS
  Fried potato skins from commercial potatoes containing low/medium glycoalkaloid levels and high glycoalkaloids potatoes were fed for 20 days to interleukin 10 gene-deficient mice and dextran sodium sulfate-induced colitic mice. Intestinal permeability, mucosal cytokine and myeloperoxidase levels and body weight were determined to assess intestinal injury.
  
  
  RESULTS
  Deep frying potato skins markedly increased glycoalkaloid content. Interleukin 10 gene-deficient mice fed fried commercial potato skins with medium glycoalkaloid content exhibited significantly elevated levels of ileal IFN-γ relative to controls. Mice in the dextran sodium sulfate colitis model that were fed the same strain of potatoes demonstrated significantly elevated levels of pro-inflammatory cytokines IFN-γ, TNF-α, and IL-17 in the colon in addition to an enhanced colonic permeability. Inflammatory response was intensified when the mice were fed potatoes with higher glycoalkaloid contents.
  
  
  CONCLUSIONS
  Our results demonstrate that consumption of potato skins containing glycoalkaloids can significantly aggravate intestinal inflammation in predisposed individuals.
authors.affiliation: Division of Gastroenterology, University of Alberta, Zeidler Ledcor Building, Edmonton, Alberta, Canada. vadim.iablokov@ucalgary.ca
authors.forename: Vadim
authors.initials: V
authors.lastname: Iablokov
authors.forename: Beate C
authors.initials: BC
authors.lastname: Sydora
authors.forename: Rae
authors.initials: R
authors.lastname: Foshaug
authors.forename: Jon
authors.initials: J
authors.lastname: Meddings
authors.forename: Darcy
authors.initials: D
authors.lastname: Driedger
authors.forename: Tom
authors.initials: T
authors.lastname: Churchill
authors.forename: Richard N
authors.initials: RN
authors.lastname: Fedorak
mesh_terms: D000818:Animals; D003093:Colitis, Ulcerative; D003296:Cooking; D003424:Crohn Disease / Q000503:physiopathology*; D016207:Cytokines / Q000032:analysis; D016264:Dextran Sulfate / Q000009:adverse effects; D004195:Disease Models, Animal; D020022:Genetic Predisposition to Disease; D015212:Inflammatory Bowel Diseases / Q000139:chemically induced / Q000235:genetics / Q000503:physiopathology*; D007413:Intestinal Mucosa / Q000378:metabolism; D051379:Mice; D009195:Peroxidase / Q000032:analysis; D012991:Solanaceous Alkaloids / Q000009:adverse effects*; D012992:Solanine / Q000031:analogs & derivatives / Q000032:analysis; D011198:Solanum tuberosum / Q000737:chemistry*
chemical_list: D016207:Cytokines; D012991:Solanaceous Alkaloids; D012992:Solanine; C011860:alpha-chaconine; D016264:Dextran Sulfate; D009195:Peroxidase