title: Attenuation of colonic inflammation by partial replacement of dietary linoleic acid with α-linolenic acid in a rat model of inflammatory bowel disease.
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.
authors.affiliation: Department of Lipid Chemistry, National Institute of Nutrition, Indian Council of Medical Research, Hyderabad, India.
authors.forename: Anupama
authors.initials: A
authors.lastname: Tyagi
authors.forename: Uday
authors.initials: U
authors.lastname: Kumar
authors.forename: Suryam
authors.initials: S
authors.lastname: Reddy
authors.forename: Vadakattu S
authors.initials: VS
authors.lastname: Santosh
authors.forename: Saazida B
authors.initials: SB
authors.lastname: Mohammed
authors.forename: Nasreen Z
authors.initials: NZ
authors.lastname: Ehtesham
authors.forename: Ahamed
authors.initials: A
authors.lastname: Ibrahim
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000627:therapeutic use; D015415:Biomarkers / Q000378:metabolism; D003092:Colitis / Q000276:immunology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D003106:Colon / Q000254:growth & development / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D016207:Cytokines / Q000378:metabolism; D016264:Dextran Sulfate; D019587:Dietary Supplements; D004195:Disease Models, Animal; D015525:Fatty Acids, Omega-3 / Q000378:metabolism; D043371:Fatty Acids, Omega-6 / Q000378:metabolism; D015212:Inflammatory Bowel Diseases / Q000276:immunology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D007413:Intestinal Mucosa / Q000254:growth & development / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D019787:Linoleic Acid / Q000008:administration & dosage; D008297:Male; D020556:Neutrophil Infiltration; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012720:Severity of Illness Index; D014886:Weaning; D017962:alpha-Linolenic Acid / Q000008:administration & dosage / Q000627:therapeutic use*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D015415:Biomarkers; D016207:Cytokines; D015525:Fatty Acids, Omega-3; D043371:Fatty Acids, Omega-6; D017962:alpha-Linolenic Acid; D016264:Dextran Sulfate; D019787:Linoleic Acid