Fish oil-enriched diet is mucosal protective against acetic acid-induced colitis in rats

Empey, Lonnie R.; Jewell, Laurence D.; Garg, Manohar L.; Thomson, A. B. R.; Clandinin, M. T.; Fedorak, Richard N.

doi:10.1139/y91-072

Cited by 54 publications

(29 citation statements)

References 27 publications

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“…LTB 4 may promote the infiltration of leukocytes into intestinal tissue and exacerbate the degree of injury. Previous studies have demonstrated that LTB 4 plays an important role in inflammatory bowel diseases [21,22].…”

Section: Discussionmentioning

confidence: 99%

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Effect of Dietary n–3 Fatty Acids on Hypoxia-Induced Necrotizing Enterocolitis in Young Mice

Akısü

Baka²,

Çoker³

et al. 1998

Neonatology

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Necrotizing entercolitis (NEC) is an important neonatal disease with a high mortality rate. Inflammatory mediators, such as mainly platelet-activating factor (PAF), leukotrienes (LT) and tumor necrosis factor play an important role in the genesis of NEC. Diets in Ω–3 (n–3) fatty acids appear to have an antiinflammatory effect, which is thought to be due to decreased active prostaglandins and leukotrienes production after incorporation of these fatty acids into cell membrane phospholipids. We investigated the protective effect of fish oil (source of n–3 fatty acids) on hypoxia-induced model of NEC. Young mice were divided into three groups; group 1 mice were fed standard chow (n–3 fatty acids-free), group 2 was fed a chow supplemented by 10% fish oil for 4 weeks. Group 3 mice served as control. We examined the intestinal lesions by light microscopy and measured intestinal tissue PAF and LB₄ levels in hypoxia-induced model of NEC. Significantly increased intestinal PAF and LTB₄ levels were found in group 1 mice when compared to group 2 and group 3 mice. The histopathology of the intestinal lesions in group 1 animals was characteristic of ischemic injury. In the n–3 fatty acids-supplemented animals these lesions were milder. The present study shows that endogenously released PAF and LTB₄ play an important role in mediating hypoxia-induced intestinal necrosis. The present study also suggests that dietary supplementation with n–3 fatty acids suppress intestinal PAF and LTB₄ generation in hypoxia-induced bowel necrosis. The intestinal protective effect of n–3 fatty acids in an experimental model of NEC may open new insight into the treatment and preventation of NEC in neonates.

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Section: Discussionmentioning

confidence: 99%

“…Dietary n-3 fatty acids have been shown to inhibit production of LTB 4 and to increase LTB 5 , which is the analogous EPA-derived metabolite [21,22]. LTB 5 is significantly less potent than LTB 4 in terms of chemotactic activity and its ability to promote neutrophil aggregation and degranulation [23].…”

Section: Discussionmentioning

confidence: 99%

Effect of Dietary n–3 Fatty Acids on Hypoxia-Induced Necrotizing Enterocolitis in Young Mice

Akısü

Baka²,

Çoker³

et al. 1998

Neonatology

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“…In addition, high levels of dietary fiber have been shown to decrease the RR for Crohn’s disease [84]. As a possible explanation, in a mouse model of colitis, dietary fiber was shown to decrease the production of TNF-a [85].…”

Section: Association Between Colorectal Cancer Inflammatory Bowel DImentioning

confidence: 99%

Nutritional Influences in Selected Gastrointestinal Diseases

Lakatos

Kiss

Miheller

2011

Dig Dis

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Nutritional factors, as sources of luminal antigens, have been thought to be important factors in the immunopathogenesis of numerous gastrointestinal diseases. In some diseases, the role of the nutritional component is causal in the susceptible host. Such diseases include celiac disease, a common heritable chronic inflammatory condition of the small intestine induced by dietary wheat, rye and barley, in susceptible individuals. Specific HLA-DQ2 and HLA-DQ8 risk alleles are necessary, but not sufficient, for disease development. The well-defined role of HLA-DQ heterodimers encoded by these alleles is to present cereal peptides to CD4+ T cells, activating an inflammatory immune response in the intestine. Genome-wide association studies have been performed which identified the IL2-IL21 risk locus and other genes with immune functions and key roles in thymic T-cell selection. Another example for this group is Wilson’s disease, an autosomal recessive disorder of copper metabolism caused by mutation of the ATP7B gene, resulting in a defect of biliary copper excretion and toxic accumulation in the body, especially in the liver, brain and cornea, resulting in hepatic and/or neurological symptoms. In other diseases, however, the association is less well established. In such endeavor, epidemiological observations may become a valuable part of the overall investigations aimed at identifying dietary factors, which are involved in the initiation and perpetuation of the specific disease. As an example, relationships between nutrition and colorectal cancer have been hypothesized early on (e.g. folate, calcium, vitamin D, red meat). Similarly, intake of certain diet constituents like fat, refined sugar, fruits, vegetables and fiber was reported to be associated with the expression of inflammatory bowel diseases. In addition, in children with active Crohn’s disease, enteral nutrition was found to be equally effective as corticosteroids in induction of remission, with mucosal healing induced by downregulation of mucosal pro-inflammatory cytokine profiles in both the ileum and the colon after enteral nutrition. However, the particular effect of the consumption of each type of food remains questionable in most cases, at least in part because of insufficient data and serious methodological limitations (e.g. recall bias, heterogeneity between collected data, lack of correction for covariates, difficulties in double blinding).

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“…The effects of dietary PUFA supplementation on disease severity are related to the production of proinflammatory eicosanoids. Four studies have found decreased colon or ileum damage and inflammation compared to n-6 PUFA diet in a rat model of chemically-induced colitis (Vilaseca et al, 1990;Empey et al, 1991;Yuceyar et al, 1999;Nieto et al, 2002). Vilaseca et al, (1990) compared the effects of dietary supplementation with either sunflower (n-6) or cod liver (n-3) oil on the development of chronic granulomatous lesions in the colon of a TNBS rat model.…”

Section: Inflammatory Lesions and Mediator Productionmentioning

confidence: 99%

“…The study concluded that the fish oil diet prevented the TXB 2 increase in the chronic stage of inflammation. Further evidence for protective effects of a fish oil (EPA)-enriched diet is shown by histological improvements in colon and ileum mucosa of rats challenged with 4% acetic acid to induce colitis (Empey et al, 1991).…”

Section: Inflammatory Lesions and Mediator Productionmentioning

confidence: 99%

Study of the effects of dietary polyunsaturated fatty acids: Molecular mechanisms involved in intestinal inflammation

Knoch¹,

Barnett²,

Roy³

et al. 2008

Grasas y Aceites

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RESUMENEstudio del efecto de los ácidos grasos poliinsaturados de la dieta: Mecanismos moleculares involucrados en la inflamación intestinal.El uso de técnicas «omic» en combinación con sistemas modelo y herramientas moleculares nos permiten entender como los alimentos y sus componentes actúan en las rutas metabólicas que regulan los procesos transcripcionales. Los ácidos grasos poliinsaturados tienen efectos nutricionales y metabólicos diferenciadores porque producen una elevación de los productos regulados por lípidos y afectan a la expresión de varios genes involucrados en la inflamación intestinal. La presente revisión se enfoca en los efectos moleculares de los ácidos grasos poliinsaturados de la dieta en la inflamación intestinal.PALABRAS CLAVE: Ácidos grasos poliinsaturados n-3 y n-6 de la dieta -Gen -Inflamación intestinal. SUMMARY Study of the effects of dietary polyunsaturated fatty acids: Molecular mechanisms involved in intestinal inflammation.The use of "omics" techniques in combination with model systems and molecular tools allows to understand how foods and food components act on metabolic pathways to regulate transcriptional processes. Polyunsaturated fatty acids have distinctive nutritional and metabolic effects because they give rise to lipid mediated products and affect the expression of various genes involved in intestinal inflammation. The present review focuses on the molecular effects of dietary polyunsaturated fatty acids on intestinal inflammation. KEY-WORDS: Dietary n-3 and n-6 polyunsaturated fatty acid -Gene -Intestinal inflammation.

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Fish oil-enriched diet is mucosal protective against acetic acid-induced colitis in rats

Cited by 54 publications

References 27 publications

Effect of Dietary n–3 Fatty Acids on Hypoxia-Induced Necrotizing Enterocolitis in Young Mice

Effect of Dietary n–3 Fatty Acids on Hypoxia-Induced Necrotizing Enterocolitis in Young Mice

Nutritional Influences in Selected Gastrointestinal Diseases

Study of the effects of dietary polyunsaturated fatty acids: Molecular mechanisms involved in intestinal inflammation

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