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Biomarkers for personalizing omega-3 fatty acid dosing.

Identifieur interne : 003A20 ( PubMed/Checkpoint ); précédent : 003A19; suivant : 003A21

Biomarkers for personalizing omega-3 fatty acid dosing.

Auteurs : Yan Jiang [États-Unis] ; Zora Djuric [États-Unis] ; Ananda Sen [États-Unis] ; Jianwei Ren [États-Unis] ; Dmitry Kuklev [États-Unis] ; Ian Waters [États-Unis] ; Lili Zhao [États-Unis] ; Charis L. Uhlson [États-Unis] ; Yu H. Hong [États-Unis] ; Robert C. Murphy [États-Unis] ; Daniel P. Normolle [États-Unis] ; William L. Smith [États-Unis] ; Dean E. Brenner [États-Unis]

Source :

RBID : pubmed:25139294

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English descriptors

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


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<term>Animals</term>
<term>Biomarkers, Tumor (analysis)</term>
<term>Body Weight</term>
<term>Colon (metabolism)</term>
<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>
<term>Inflammation</term>
<term>Lipids (chemistry)</term>
<term>Male</term>
<term>Models, Theoretical</term>
<term>Phospholipids (chemistry)</term>
<term>Rats</term>
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</keywords>
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<term>Acides gras ()</term>
<term>Acides gras omega-3 (métabolisme)</term>
<term>Animaux</term>
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<term>Dinoprostone (urine)</term>
<term>Huiles de poisson</term>
<term>Hydroquinones ()</term>
<term>Inflammation</term>
<term>Lipides ()</term>
<term>Marqueurs biologiques tumoraux (analyse)</term>
<term>Modèles théoriques</term>
<term>Mâle</term>
<term>Phospholipides ()</term>
<term>Poids du corps</term>
<term>Rats</term>
<term>Rats de lignée F344</term>
<term>Spectrométrie de masse en tandem</term>
<term>Température</term>
<term>Éicosanoïdes (métabolisme)</term>
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<term>Biomarkers, Tumor</term>
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<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en">
<term>Fatty Acids</term>
<term>Hydroquinones</term>
<term>Lipids</term>
<term>Phospholipids</term>
</keywords>
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<term>Marqueurs biologiques tumoraux</term>
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<term>Colon</term>
<term>Eicosanoids</term>
<term>Fatty Acids, Omega-3</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>Acides gras omega-3</term>
<term>Côlon</term>
<term>Éicosanoïdes</term>
</keywords>
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<term>Dinoprostone</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Animals</term>
<term>Body Weight</term>
<term>Fish Oils</term>
<term>Gas Chromatography-Mass Spectrometry</term>
<term>Inflammation</term>
<term>Male</term>
<term>Models, Theoretical</term>
<term>Rats</term>
<term>Rats, Inbred F344</term>
<term>Tandem Mass Spectrometry</term>
<term>Temperature</term>
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<term>Acides gras</term>
<term>Animaux</term>
<term>Chromatographie gazeuse-spectrométrie de masse</term>
<term>Dinoprostone</term>
<term>Huiles de poisson</term>
<term>Hydroquinones</term>
<term>Inflammation</term>
<term>Lipides</term>
<term>Modèles théoriques</term>
<term>Mâle</term>
<term>Phospholipides</term>
<term>Poids du corps</term>
<term>Rats</term>
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<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>
</Abstract>
<AuthorList CompleteYN="Y">
<Author ValidYN="Y">
<LastName>Jiang</LastName>
<ForeName>Yan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo>
<Affiliation>Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Djuric</LastName>
<ForeName>Zora</ForeName>
<Initials>Z</Initials>
<AffiliationInfo>
<Affiliation>Department of Family Medicine, University of Michigan Medical School, Ann Arbor, Michigan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Sen</LastName>
<ForeName>Ananda</ForeName>
<Initials>A</Initials>
<AffiliationInfo>
<Affiliation>Department of Family Medicine, University of Michigan Medical School, Ann Arbor, Michigan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Ren</LastName>
<ForeName>Jianwei</ForeName>
<Initials>J</Initials>
<AffiliationInfo>
<Affiliation>Department of Family Medicine, University of Michigan Medical School, Ann Arbor, Michigan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Kuklev</LastName>
<ForeName>Dmitry</ForeName>
<Initials>D</Initials>
<AffiliationInfo>
<Affiliation>Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, Michigan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Waters</LastName>
<ForeName>Ian</ForeName>
<Initials>I</Initials>
<AffiliationInfo>
<Affiliation>Department of Family Medicine, University of Michigan Medical School, Ann Arbor, Michigan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Zhao</LastName>
<ForeName>Lili</ForeName>
<Initials>L</Initials>
<AffiliationInfo>
<Affiliation>Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, Michigan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Uhlson</LastName>
<ForeName>Charis L</ForeName>
<Initials>CL</Initials>
<AffiliationInfo>
<Affiliation>Department of Pharmacology, University of Colorado Denver, Aurora, Colorado.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Hong</LastName>
<ForeName>Yu H</ForeName>
<Initials>YH</Initials>
<AffiliationInfo>
<Affiliation>Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, Michigan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Murphy</LastName>
<ForeName>Robert C</ForeName>
<Initials>RC</Initials>
<AffiliationInfo>
<Affiliation>Department of Pharmacology, University of Colorado Denver, Aurora, Colorado.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Normolle</LastName>
<ForeName>Daniel P</ForeName>
<Initials>DP</Initials>
<AffiliationInfo>
<Affiliation>Department of Biostatistics, University of Pittsburgh, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Smith</LastName>
<ForeName>William L</ForeName>
<Initials>WL</Initials>
<AffiliationInfo>
<Affiliation>Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, Michigan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Brenner</LastName>
<ForeName>Dean E</ForeName>
<Initials>DE</Initials>
<AffiliationInfo>
<Affiliation>Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan. Department of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan. VA Medical Center, Ann Arbor, Michigan. dbrenner@med.umich.edu.</Affiliation>
</AffiliationInfo>
</Author>
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<Agency>NHLBI NIH HHS</Agency>
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<Agency>NIDDK NIH HHS</Agency>
<Country>United States</Country>
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<Grant>
<GrantID>M01 RR000042</GrantID>
<Acronym>RR</Acronym>
<Agency>NCRR NIH HHS</Agency>
<Country>United States</Country>
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<GrantID>AT002782</GrantID>
<Acronym>AT</Acronym>
<Agency>NCCIH NIH HHS</Agency>
<Country>United States</Country>
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<Grant>
<GrantID>P50 AT002782</GrantID>
<Acronym>AT</Acronym>
<Agency>NCCIH NIH HHS</Agency>
<Country>United States</Country>
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<Grant>
<GrantID>CA130810</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant>
<GrantID>R01 GM068848</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
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<Year>2014</Year>
<Month>08</Month>
<Day>19</Day>
</ArticleDate>
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<Country>United States</Country>
<MedlineTA>Cancer Prev Res (Phila)</MedlineTA>
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<QualifierName UI="Q000032" MajorTopicYN="Y">analysis</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D001835" MajorTopicYN="N">Body Weight</DescriptorName>
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<MeshHeading>
<DescriptorName UI="D003106" MajorTopicYN="N">Colon</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<DescriptorName UI="D015232" MajorTopicYN="N">Dinoprostone</DescriptorName>
<QualifierName UI="Q000652" MajorTopicYN="N">urine</QualifierName>
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<DescriptorName UI="D015777" MajorTopicYN="N">Eicosanoids</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading>
<DescriptorName UI="D005227" MajorTopicYN="N">Fatty Acids</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
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<MeshHeading>
<DescriptorName UI="D015525" MajorTopicYN="N">Fatty Acids, Omega-3</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
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<DescriptorName UI="D005395" MajorTopicYN="N">Fish Oils</DescriptorName>
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<DescriptorName UI="D008401" MajorTopicYN="N">Gas Chromatography-Mass Spectrometry</DescriptorName>
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<DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName>
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<DescriptorName UI="D008055" MajorTopicYN="N">Lipids</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
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<DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
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<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
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<DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName>
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<DescriptorName UI="D011916" MajorTopicYN="N">Rats, Inbred F344</DescriptorName>
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<MeshHeading>
<DescriptorName UI="D053719" MajorTopicYN="N">Tandem Mass Spectrometry</DescriptorName>
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<name sortKey="Hong, Yu H" sort="Hong, Yu H" uniqKey="Hong Y" first="Yu H" last="Hong">Yu H. Hong</name>
<name sortKey="Kuklev, Dmitry" sort="Kuklev, Dmitry" uniqKey="Kuklev D" first="Dmitry" last="Kuklev">Dmitry Kuklev</name>
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<name sortKey="Ren, Jianwei" sort="Ren, Jianwei" uniqKey="Ren J" first="Jianwei" last="Ren">Jianwei Ren</name>
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<name sortKey="Smith, William L" sort="Smith, William L" uniqKey="Smith W" first="William L" last="Smith">William L. Smith</name>
<name sortKey="Uhlson, Charis L" sort="Uhlson, Charis L" uniqKey="Uhlson C" first="Charis L" last="Uhlson">Charis L. Uhlson</name>
<name sortKey="Waters, Ian" sort="Waters, Ian" uniqKey="Waters I" first="Ian" last="Waters">Ian Waters</name>
<name sortKey="Zhao, Lili" sort="Zhao, Lili" uniqKey="Zhao L" first="Lili" last="Zhao">Lili Zhao</name>
</country>
</tree>
</affiliations>
</record>

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