Dataset Information

Dietary fish oil supplementation inhibits formation of endometriosis-associated adhesions in a chimeric mouse model.

ABSTRACT:

Objective

To examine whether dietary fish oil supplementation reduces development of spontaneous endometriosis-associated adhesions using an established model.

Design

Laboratory-based study.

Setting

Medical center research laboratory. PATIENT(S)/ANIMAL(S): Disease-free women of reproductive age and nude mice.

Intervention(s)

Women were not provided any intervention. Mice were randomized to receive fish oil supplementation or control diet.

Main outcome measure(s)

Experimental endometriosis was established in mice via injection of human endometrial tissue within 16 hours of ovariectomy. Mice were provided standard or menhaden fish oil-supplemented diets for ? 2 weeks before initiation of experimental endometriosis and until killing them 1 week later. At necropsy, mice were examined for the presence and extent of adhesions and endometriotic-like lesions. Tissues were excised and morphologically characterized.

Result(s)

Adhesions/lesions were reduced in mice provided with dietary fish oil compared with control animals. Leukocytes were more numerous within the adhesions/lesions of the mice maintained on the standard diet compared with animals provided with fish oil. As indicated by staining intensity, collagen deposition was greater at adhesion sites within control mice compared with fish oil-supplemented animals.

Conclusion(s)

Wound-healing associated with surgery created an inflammatory peritoneal microenvironment that promoted the development of both experimental endometriosis and adhesions in a murine model. Targeting excessive inflammation with fish oil may be an effective adjuvant therapy to reduce the development of postsurgical adhesions related to endometriosis.

SUBMITTER: Herington JL

PROVIDER: S-EPMC3582352 | biostudies-literature | 2013 Feb

REPOSITORIES: biostudies-literature

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Publications

Dietary fish oil supplementation inhibits formation of endometriosis-associated adhesions in a chimeric mouse model.

Herington Jennifer L JL Glore Dana R DR Lucas John A JA Osteen Kevin G KG Bruner-Tran Kaylon L KL

Fertility and sterility 20121025 2

<h4>Objective</h4>To examine whether dietary fish oil supplementation reduces development of spontaneous endometriosis-associated adhesions using an established model.<h4>Design</h4>Laboratory-based study.<h4>Setting</h4>Medical center research laboratory. PATIENT(S)/ANIMAL(S): Disease-free women of reproductive age and nude mice.<h4>Intervention(s)</h4>Women were not provided any intervention. Mice were randomized to receive fish oil supplementation or control diet.<h4>Main outcome measure(s)</ ...[more]

PMID: 23103017

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Project description:Colorectal cancer is the second leading cause of cancer-related death within the United States. Animal models and observational studies have suggested that marine-derived n-3 polyunsaturated fatty acids [PUFA] such as eicosapentanoic acid [EPA] and docosahexanoic acid [DHA] may reduce the risk of colorectal cancer. In addition, it may be the relative proportion of n-3 to n-6 PUFAs that best determines the chemopreventive effects of fish oils. This ratio is important because the n-6 PUFA, arachidonic acid (ARA), is converted via the cyclo-oxygenase (COX) pathway to prostaglandin E2 (PGE2), an inflammatory eicosanoid overproduced in colorectal neoplasms while EPA is converted to the anti-inflammatory prostaglandin E3 (PGE3). While the ratio of n-6 to n-3 PUFAs can be altered through dietary changes, genetic factors may also influence this ratio. Recent genetic studies have demonstrated that much of the tissue levels of ARA is determined by differences in a gene called fatty acid desaturase 1 (FADS1). FADS1 is the rate-limiting enzyme in the conversion of linoleic acid, the most commonly consumed PUFA in the Western diet, to ARA, and one particular genetic variant caller rs174537 is associated with lower fatty acid desaturase activity and subsequently lower tissue levels of ARA. The study hypothesis is that individuals with genetically determined lower activity of FADS1 will derive greater benefit from fish oil supplementation than individuals with higher FADS1 activity because of lower tissue levels of ARA and subsequently a more favorable n-6 to n-3 PUFA ratio. To test this hypothesis the investigators will recruit 150 participants with recently identified adenomatous polyps and conduct a 6-month double blind 3 X 2 factorial randomized controlled trial. The first factor will be FADS1 genotype (GG, GT, and TT) and the second factor will be fish oil supplementation (fish oil versus placebo). The primary outcome will be the change in rectal epithelial cell growth and cell death. Secondary outcomes will include rectal epithelial cell expression of genes important in PGE2 production, rectal cell production of PGE2 and PGE3, rectal mucosal tissue levels of fatty acids, and changes in biomarkers of inflammation (C-reactive protein), adipokines (leptin, adiponectin), and markers of insulin sensitivity. The specific aims include: 1) to determine the efficacy of fish oil supplements on rectal epithelial cell proliferation indexes and markers of rectal crypt apoptosis, and 2) to determine the effect of genetically-determined fatty acid desaturase 1 activity on fish oil supplementation for colorectal cancer chemoprevention. The investigators long-term objectives are to determine genetic factors that might influence the efficacy of fish oil supplementation in order to conduct a more definitive adenoma recurrence trial using marine-derived n-3 PUFAs. The investigators anticipate that fish oil will have anti-neoplastic effect and individuals with low FADS1 activity will have a greater response compared to individuals with high FADS1 activity

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Dataset Information

Dietary fish oil supplementation inhibits formation of endometriosis-associated adhesions in a chimeric mouse model.

Objective

Design

Setting

Intervention(s)

Main outcome measure(s)

Result(s)

Conclusion(s)

Publications

Dietary fish oil supplementation inhibits formation of endometriosis-associated adhesions in a chimeric mouse model.

Similar Datasets

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