Attenuation of colonic inflammation by partial replacement of dietary linoleic acid with α-linolenic acid in a rat model of inflammatory bowel disease

Br J Nutr. 2012 Nov 14;108(9):1612-22. doi: 10.1017/S0007114511007197. Epub 2012 Jan 16.

Abstract

Increasing prevalence of inflammatory bowel disease may be due to imbalance in the intake of n-6 and n-3 PUFA in the diet. This study investigates the impact of varying ratios of dietary linoleic acid (LA, 18 : 2n-6) to α-linolenic acid (ALA, 18 : 3n-3) on the inflammatory response in dextran sulphate sodium (DSS)-induced colitis. Weanling male Sprague-Dawley rats were divided into five groups: a non-colitic group with a LA:ALA ratio of 215 (CON-215), and colitic groups with LA:ALA ratios of 215 (DSS-215), 50 (DSS-50), 10 (DSS-10) and 2 (DSS-2). Blends of groundnut, palmolein and linseed oils were used to provide varying LA:ALA ratios. All the rats were fed the respective experimental isoenergetic diets containing 10 % fat for 90 d and DSS was administered during the last 11 d. Colonic inflammation was evaluated by clinical, biochemical and histological parameters. The results showed attenuation of colitis in the DSS-2 group as evidenced by significant reductions in disease activity index, mucosal myeloperoxidase activity (P < 0·05), alkaline phosphatase activity (P < 0·01) and increase in colon length (P < 0·01) compared to the groups fed with higher ratios (DSS-215). This was accompanied by significant reductions in mucosal proinflammatory cytokines TNF-α (P < 0·01) and IL-1β (P < 0·01) and improvement in the histological score. Further, ALA supplementation increased long-chain (LC) n-3 PUFA and decreased LC n-6 PUFA in colon structural lipids. These data suggest that substitution of one-third of LA with ALA (LA:ALA ratio 2) mitigates experimental colitis by down-regulating proinflammatory mediators.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / administration & dosage
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Biomarkers / metabolism
  • Colitis / immunology
  • Colitis / pathology
  • Colitis / physiopathology
  • Colitis / prevention & control*
  • Colon / growth & development
  • Colon / immunology*
  • Colon / metabolism
  • Colon / pathology
  • Cytokines / metabolism
  • Dextran Sulfate
  • Dietary Supplements*
  • Disease Models, Animal*
  • Fatty Acids, Omega-3 / metabolism
  • Fatty Acids, Omega-6 / metabolism
  • Inflammatory Bowel Diseases / immunology
  • Inflammatory Bowel Diseases / pathology
  • Inflammatory Bowel Diseases / physiopathology
  • Inflammatory Bowel Diseases / prevention & control*
  • Intestinal Mucosa / growth & development
  • Intestinal Mucosa / immunology*
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / pathology
  • Linoleic Acid / administration & dosage
  • Male
  • Neutrophil Infiltration
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Severity of Illness Index
  • Weaning
  • alpha-Linolenic Acid / administration & dosage
  • alpha-Linolenic Acid / therapeutic use*

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Biomarkers
  • Cytokines
  • Fatty Acids, Omega-3
  • Fatty Acids, Omega-6
  • alpha-Linolenic Acid
  • Dextran Sulfate
  • Linoleic Acid