title: Dietary supplementation of arachidonic acid increases arachidonic acid and lipoxin A₄ contents in colon, but does not affect severity or prostaglandin E₂ content in murine colitis model.
abstract: BACKGROUND
  Arachidonic acid (ARA) is an essential fatty acid and a major constituent of biomembranes. It is converted into various lipid mediators, such as prostaglandin E₂ (PGE₂) and lipoxin A₄ (LXA₄). The effects of dietary ARA on colon maintenance are unclear because PGE₂ has both mucosal protective and proinflammatory effects, and LXA₄ has an anti-inflammatory role. Our objective is to clarify the effects of dietary ARA on an experimental murine colitis model.
  
  
  METHODS
  C57BL/6 mice were fed three types of ARA diet (0.075%, 0.15% or 0.305% ARA in diet), DHA diet (0.315% DHA) or control diet for 6 weeks, and were then administered dextran sodium sulphate (DSS) for 7 days to induce colitis. We evaluated colitis severity, fatty acid and lipid mediator contents in colonic tissue, and the expression of genes related to lipid mediator formation.
  
  
  RESULTS
  ARA composition of colon phospholipids was significantly elevated in an ARA dose-dependent manner. ARA, as well as DHA, did not affect colitis severity (body weight loss, colon shortening, diarrhea and hemoccult phenomena) and histological features. PGE₂ contents in the colon were unchanged by dietary ARA, while LXA₄ contents increased in an ARA dose-dependent manner. Gene expression of cyclooxygenase (COX)-1 and COX-2 was unchanged, while that of 12/15-lipoxgenase (LOX) was significantly increased by dietary ARA. ARA composition did not correlate with neither colon length nor PGE₂ contents, but significantly correlated with LXA₄ content.
  
  
  CONCLUSIONS
  These results suggest that dietary ARA increases ARA and LXA₄ contents in colon, but that it has no effect on severity and PGE₂ content in a DSS-induced murine colitis model.
authors: Institute for Health Care Science, Suntory Wellness Ltd, 1-1-1 Wakayamadai, Shimamoto, Osaka 6188503, Japan. norifumi_tateishi@suntory.co.jp.
authors: Norifumi
authors: N
authors: Tateishi
authors: Saki
authors: S
authors: Kakutani
authors: Hiroshi
authors: H
authors: Kawashima
authors: Hiroshi
authors: H
authors: Shibata
authors: Ikuo
authors: I
authors: Morita
mesh_terms: D000284:Administration, Oral; D000818:Animals; D016718:Arachidonic Acid / Q000008:administration & dosage* / Q000378:metabolism / Q000493:pharmacokinetics; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D003106:Colon / Q000378:metabolism* / Q000473:pathology; D016264:Dextran Sulfate; D019587:Dietary Supplements; D015232:Dinoprostone / Q000378:metabolism*; D004281:Docosahexaenoic Acids / Q000008:administration & dosage / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D044045:Lipoxins / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D010743:Phospholipids / Q000378:metabolism; D012720:Severity of Illness Index; D014018:Tissue Distribution
chemical_list: D044045:Lipoxins; D010743:Phospholipids; C040527:lipoxin A4; D004281:Docosahexaenoic Acids; D016718:Arachidonic Acid; D016264:Dextran Sulfate; D015232:Dinoprostone