Biomarkers for personalizing omega-3 fatty acid dosing.
Identifieur interne : 001903 ( PubMed/Corpus ); précédent : 001902; suivant : 001904Biomarkers for personalizing omega-3 fatty acid dosing.
Auteurs : Yan Jiang ; Zora Djuric ; Ananda Sen ; Jianwei Ren ; Dmitry Kuklev ; Ian Waters ; Lili Zhao ; Charis L. Uhlson ; Yu H. Hong ; Robert C. Murphy ; Daniel P. Normolle ; William L. Smith ; Dean E. BrennerSource :
- Cancer prevention research (Philadelphia, Pa.) [ 1940-6215 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Biomarkers, Tumor (analysis), Body Weight, Colon (metabolism), Dinoprostone (urine), Eicosanoids (metabolism), Fatty Acids (chemistry), Fatty Acids, Omega-3 (metabolism), Fish Oils, Gas Chromatography-Mass Spectrometry, Hydroquinones (chemistry), Inflammation, Lipids (chemistry), Male, Models, Theoretical, Phospholipids (chemistry), Rats, Rats, Inbred F344, Tandem Mass Spectrometry, Temperature.
- MESH :
- chemical , analysis : Biomarkers, Tumor.
- chemical , chemistry : Fatty Acids, Hydroquinones, Lipids, Phospholipids.
- metabolism : Colon, Eicosanoids, Fatty Acids, Omega-3.
- chemical , urine : Dinoprostone.
- Animals, Body Weight, Fish Oils, Gas Chromatography-Mass Spectrometry, Inflammation, Male, Models, Theoretical, Rats, Rats, Inbred F344, Tandem Mass Spectrometry, Temperature.
Abstract
Prostaglandin E2 (PGE2) has been linked to a higher risk of colorectal cancer. PGE2 in colon tissue can be reduced by increasing dietary eicosapentaenoic acid (EPA). The dose-dependent relationships between dietary EPA, serum EPA:arachidonate (AA) ratio, urinary PGE2 metabolites, and colonic eicosanoids were evaluated to develop biomarkers for prediction of colonic PGE2. Male rats were fed diets containing EPA:ω6 fatty acid ratios of 0, 0.1, 0.2, 0.4, or 0.6 for 5 weeks. Increasing the dietary EPA:ω6 fatty acid ratio increased EPA:AA ratios in serum and in the proximal, transverse, and distal colon (P < 0.001). The urinary PGE2 metabolite was reduced (P = 0.006). EPA-rich diets reduced colonic tissue PGE2 concentrations by 58% to 66% and increased PGE3 by 19- to 28-fold. Other AA-derived eicosanoids were reduced by 35% to 83%. The changes were not linear, with the largest changes in eicosanoids observed with the lower doses. A mathematical model predicts colonic tissue eicosanoids from the EPA:AA ratio in serum and the EPA dose. Every 10% increase in serum EPA:AA was associated with a 2% decrease in the (geometric) mean of PGE2 in the distal colon. These mathematical relationships can now be applied to individualized EPA dosing in clinical trials.
DOI: 10.1158/1940-6207.CAPR-14-0134
PubMed: 25139294
Links to Exploration step
pubmed:25139294Le document en format XML
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<term>Dinoprostone (urine)</term>
<term>Eicosanoids (metabolism)</term>
<term>Fatty Acids (chemistry)</term>
<term>Fatty Acids, Omega-3 (metabolism)</term>
<term>Fish Oils</term>
<term>Gas Chromatography-Mass Spectrometry</term>
<term>Hydroquinones (chemistry)</term>
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<term>Phospholipids (chemistry)</term>
<term>Rats</term>
<term>Rats, Inbred F344</term>
<term>Tandem Mass Spectrometry</term>
<term>Temperature</term>
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<term>Hydroquinones</term>
<term>Lipids</term>
<term>Phospholipids</term>
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<term>Eicosanoids</term>
<term>Fatty Acids, Omega-3</term>
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<term>Inflammation</term>
<term>Male</term>
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<front><div type="abstract" xml:lang="en">Prostaglandin E2 (PGE2) has been linked to a higher risk of colorectal cancer. PGE2 in colon tissue can be reduced by increasing dietary eicosapentaenoic acid (EPA). The dose-dependent relationships between dietary EPA, serum EPA:arachidonate (AA) ratio, urinary PGE2 metabolites, and colonic eicosanoids were evaluated to develop biomarkers for prediction of colonic PGE2. Male rats were fed diets containing EPA:ω6 fatty acid ratios of 0, 0.1, 0.2, 0.4, or 0.6 for 5 weeks. Increasing the dietary EPA:ω6 fatty acid ratio increased EPA:AA ratios in serum and in the proximal, transverse, and distal colon (P < 0.001). The urinary PGE2 metabolite was reduced (P = 0.006). EPA-rich diets reduced colonic tissue PGE2 concentrations by 58% to 66% and increased PGE3 by 19- to 28-fold. Other AA-derived eicosanoids were reduced by 35% to 83%. The changes were not linear, with the largest changes in eicosanoids observed with the lower doses. A mathematical model predicts colonic tissue eicosanoids from the EPA:AA ratio in serum and the EPA dose. Every 10% increase in serum EPA:AA was associated with a 2% decrease in the (geometric) mean of PGE2 in the distal colon. These mathematical relationships can now be applied to individualized EPA dosing in clinical trials.</div>
</front>
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<Abstract><AbstractText>Prostaglandin E2 (PGE2) has been linked to a higher risk of colorectal cancer. PGE2 in colon tissue can be reduced by increasing dietary eicosapentaenoic acid (EPA). The dose-dependent relationships between dietary EPA, serum EPA:arachidonate (AA) ratio, urinary PGE2 metabolites, and colonic eicosanoids were evaluated to develop biomarkers for prediction of colonic PGE2. Male rats were fed diets containing EPA:ω6 fatty acid ratios of 0, 0.1, 0.2, 0.4, or 0.6 for 5 weeks. Increasing the dietary EPA:ω6 fatty acid ratio increased EPA:AA ratios in serum and in the proximal, transverse, and distal colon (P < 0.001). The urinary PGE2 metabolite was reduced (P = 0.006). EPA-rich diets reduced colonic tissue PGE2 concentrations by 58% to 66% and increased PGE3 by 19- to 28-fold. Other AA-derived eicosanoids were reduced by 35% to 83%. The changes were not linear, with the largest changes in eicosanoids observed with the lower doses. A mathematical model predicts colonic tissue eicosanoids from the EPA:AA ratio in serum and the EPA dose. Every 10% increase in serum EPA:AA was associated with a 2% decrease in the (geometric) mean of PGE2 in the distal colon. These mathematical relationships can now be applied to individualized EPA dosing in clinical trials.</AbstractText>
<CopyrightInformation>©2014 American Association for Cancer Research.</CopyrightInformation>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jiang</LastName>
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<MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName>
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<MeshHeading><DescriptorName UI="D008055" MajorTopicYN="N">Lipids</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
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<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
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