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Oleic Acid Attenuates trans-10,cis-12 Conjugated Linoleic Acid-Mediated Inflammatory Gene Expression in Human Adipocytes
The weight loss supplement conjugated linoleic acid (CLA) consists of an equal mixture of trans -10, cis -12 (10,12) and cis -9, trans -11 (9,11) isomers. However, high levels of mixed CLA isomers, or the 10,12 isomer, causes chronic inflammation, lipodystrophy, or insulin resistance. We previously...
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Published in: | Lipids 2012-11, Vol.47 (11), p.1043-1051 |
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creator | Reardon, Meaghan Gobern, Semone Martinez, Kristina Shen, Wan Reid, Tanya McIntosh, Michael |
description | The weight loss supplement conjugated linoleic acid (CLA) consists of an equal mixture of
trans
-10,
cis
-12 (10,12) and
cis
-9,
trans
-11 (9,11) isomers. However, high levels of mixed CLA isomers, or the 10,12 isomer, causes chronic inflammation, lipodystrophy, or insulin resistance. We previously demonstrated that 10,12 CLA decreases de novo lipid synthesis along with the abundance and activity of stearoyl-CoA desaturase (SCD)-1, a δ-9 desaturase essential for the synthesis of monounsaturated fatty acids (MUFA). Thus, we hypothesized that the 10,12 CLA-mediated decrease in SCD-1, with the subsequent decrease in MUFA, was responsible for the observed effects. To test this hypothesis, 10,12 CLA-treated human adipocytes were supplemented with oleic acid for 12 h to 7 days, and inflammatory gene expression, insulin-stimulated glucose uptake, and lipid content were measured. Oleic acid reduced inflammatory gene expression in a dose-dependent manner, and restored the lipid content of 10,12 CLA-treated adipocytes without improving insulin-stimulated glucose uptake. In contrast, supplementation with stearic acid, a substrate for SCD-1, or 9,11 CLA did not prevent inflammatory gene expression by 10,12 CLA. Notably, 10,12 CLA impacted the expression of several G-protein coupled receptors that was attenuated by oleic acid. Collectively, these data show that oleic acid attenuates 10,12 CLA-induced inflammatory gene expression and lipid content, possibly by alleviating cell stress caused by the inhibition of MUFA needed for phospholipid and neutral lipid synthesis. |
doi_str_mv | 10.1007/s11745-012-3711-0 |
format | article |
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trans
-10,
cis
-12 (10,12) and
cis
-9,
trans
-11 (9,11) isomers. However, high levels of mixed CLA isomers, or the 10,12 isomer, causes chronic inflammation, lipodystrophy, or insulin resistance. We previously demonstrated that 10,12 CLA decreases de novo lipid synthesis along with the abundance and activity of stearoyl-CoA desaturase (SCD)-1, a δ-9 desaturase essential for the synthesis of monounsaturated fatty acids (MUFA). Thus, we hypothesized that the 10,12 CLA-mediated decrease in SCD-1, with the subsequent decrease in MUFA, was responsible for the observed effects. To test this hypothesis, 10,12 CLA-treated human adipocytes were supplemented with oleic acid for 12 h to 7 days, and inflammatory gene expression, insulin-stimulated glucose uptake, and lipid content were measured. Oleic acid reduced inflammatory gene expression in a dose-dependent manner, and restored the lipid content of 10,12 CLA-treated adipocytes without improving insulin-stimulated glucose uptake. In contrast, supplementation with stearic acid, a substrate for SCD-1, or 9,11 CLA did not prevent inflammatory gene expression by 10,12 CLA. Notably, 10,12 CLA impacted the expression of several G-protein coupled receptors that was attenuated by oleic acid. Collectively, these data show that oleic acid attenuates 10,12 CLA-induced inflammatory gene expression and lipid content, possibly by alleviating cell stress caused by the inhibition of MUFA needed for phospholipid and neutral lipid synthesis.</description><identifier>ISSN: 0024-4201</identifier><identifier>EISSN: 1558-9307</identifier><identifier>DOI: 10.1007/s11745-012-3711-0</identifier><identifier>PMID: 22941440</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Adipocytes ; Adipocytes - drug effects ; Adipocytes - metabolism ; Adult ; Biomedical and Life Sciences ; Cells, Cultured ; Conjugated linoleic acid ; Dietary Supplements ; dose response ; Dose-Response Relationship, Drug ; Fatty Acids, Monounsaturated - antagonists & inhibitors ; Female ; G-protein coupled receptors ; gene expression ; Gene Expression - drug effects ; glucose ; G‐protein receptors ; Humans ; inflammation ; Inflammation - drug therapy ; Inflammation - genetics ; Inflammation - metabolism ; Inflammatory gene expression ; insulin resistance ; isomers ; Life Sciences ; Linoleic Acids, Conjugated - administration & dosage ; Linoleic Acids, Conjugated - pharmacology ; lipid content ; Lipidology ; Medical Biochemistry ; Medicinal Chemistry ; Microbial Genetics and Genomics ; Middle Aged ; Monounsaturated fatty acids ; Neurochemistry ; Nutrition ; Oleic acid ; Oleic Acids - pharmacology ; Original Article ; phospholipids ; stearic acid ; Stearoyl-CoA Desaturase - antagonists & inhibitors ; Stearoyl-CoA Desaturase - metabolism ; Stearoyl‐CoA desaturase ; Structure-Activity Relationship ; weight loss ; Young Adult</subject><ispartof>Lipids, 2012-11, Vol.47 (11), p.1043-1051</ispartof><rights>AOCS 2012</rights><rights>2012 American Oil Chemists' Society (AOCS)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5843-1b5441dfe48a9d4b5fd6b03371341b5289b5339e7402349fd1644c9d8a7a452e3</citedby><cites>FETCH-LOGICAL-c5843-1b5441dfe48a9d4b5fd6b03371341b5289b5339e7402349fd1644c9d8a7a452e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11745-012-3711-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11745-012-3711-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,1638,27901,27902,41394,42463,51293</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22941440$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reardon, Meaghan</creatorcontrib><creatorcontrib>Gobern, Semone</creatorcontrib><creatorcontrib>Martinez, Kristina</creatorcontrib><creatorcontrib>Shen, Wan</creatorcontrib><creatorcontrib>Reid, Tanya</creatorcontrib><creatorcontrib>McIntosh, Michael</creatorcontrib><title>Oleic Acid Attenuates trans-10,cis-12 Conjugated Linoleic Acid-Mediated Inflammatory Gene Expression in Human Adipocytes</title><title>Lipids</title><addtitle>Lipids</addtitle><addtitle>Lipids</addtitle><description>The weight loss supplement conjugated linoleic acid (CLA) consists of an equal mixture of
trans
-10,
cis
-12 (10,12) and
cis
-9,
trans
-11 (9,11) isomers. However, high levels of mixed CLA isomers, or the 10,12 isomer, causes chronic inflammation, lipodystrophy, or insulin resistance. We previously demonstrated that 10,12 CLA decreases de novo lipid synthesis along with the abundance and activity of stearoyl-CoA desaturase (SCD)-1, a δ-9 desaturase essential for the synthesis of monounsaturated fatty acids (MUFA). Thus, we hypothesized that the 10,12 CLA-mediated decrease in SCD-1, with the subsequent decrease in MUFA, was responsible for the observed effects. To test this hypothesis, 10,12 CLA-treated human adipocytes were supplemented with oleic acid for 12 h to 7 days, and inflammatory gene expression, insulin-stimulated glucose uptake, and lipid content were measured. Oleic acid reduced inflammatory gene expression in a dose-dependent manner, and restored the lipid content of 10,12 CLA-treated adipocytes without improving insulin-stimulated glucose uptake. In contrast, supplementation with stearic acid, a substrate for SCD-1, or 9,11 CLA did not prevent inflammatory gene expression by 10,12 CLA. Notably, 10,12 CLA impacted the expression of several G-protein coupled receptors that was attenuated by oleic acid. Collectively, these data show that oleic acid attenuates 10,12 CLA-induced inflammatory gene expression and lipid content, possibly by alleviating cell stress caused by the inhibition of MUFA needed for phospholipid and neutral lipid synthesis.</description><subject>Adipocytes</subject><subject>Adipocytes - drug effects</subject><subject>Adipocytes - metabolism</subject><subject>Adult</subject><subject>Biomedical and Life Sciences</subject><subject>Cells, Cultured</subject><subject>Conjugated linoleic acid</subject><subject>Dietary Supplements</subject><subject>dose response</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fatty Acids, Monounsaturated - antagonists & inhibitors</subject><subject>Female</subject><subject>G-protein coupled receptors</subject><subject>gene expression</subject><subject>Gene Expression - drug effects</subject><subject>glucose</subject><subject>G‐protein receptors</subject><subject>Humans</subject><subject>inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - genetics</subject><subject>Inflammation - metabolism</subject><subject>Inflammatory gene expression</subject><subject>insulin resistance</subject><subject>isomers</subject><subject>Life Sciences</subject><subject>Linoleic Acids, Conjugated - administration & dosage</subject><subject>Linoleic Acids, Conjugated - pharmacology</subject><subject>lipid content</subject><subject>Lipidology</subject><subject>Medical Biochemistry</subject><subject>Medicinal Chemistry</subject><subject>Microbial Genetics and Genomics</subject><subject>Middle Aged</subject><subject>Monounsaturated fatty acids</subject><subject>Neurochemistry</subject><subject>Nutrition</subject><subject>Oleic acid</subject><subject>Oleic Acids - pharmacology</subject><subject>Original Article</subject><subject>phospholipids</subject><subject>stearic acid</subject><subject>Stearoyl-CoA Desaturase - antagonists & inhibitors</subject><subject>Stearoyl-CoA Desaturase - metabolism</subject><subject>Stearoyl‐CoA desaturase</subject><subject>Structure-Activity Relationship</subject><subject>weight loss</subject><subject>Young Adult</subject><issn>0024-4201</issn><issn>1558-9307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNqNkkGP0zAQhS0EYkvhB3BBlrhwIOCxx-vkglSVZbdS0XKAs-XGTnGV2CVOlu2_xyVLtSAhOFn2fO95xn6EPAf2BhhTbxOAQlkw4IVQAAV7QGYgZVlUgqmHZMYYxwI5gzPyJKVd3gJW8jE547xCQGQzcnvdOl_TRe0tXQyDC6MZXKJDb0IqgL2ufV44XcawG7e5ZOnah3jSFB-d9T-PV6FpTdeZIfYHeumCoxe3-96l5GOgPtCrsTOBLqzfx_qQr3hKHjWmTe7Z3TonXz5cfF5eFevry9VysS5qWaIoYCMRwTYOS1NZ3MjGnm-YyOMKzDVeVhspROUUMi6waiycI9aVLY0yKLkTc_Ju8t2Pm87Z2oU8W6v3ve9Mf9DReP17JfivehtvtEBVCc6zwas7gz5-G10adOdT7drWBBfHpEFJgSUvmfwPVIgMV9l4Tl7-ge7i2If8EhoAkJeg4EjBRNV9TKl3zalvYPoYAT1FQOcI6GMENMuaF_cHPil-_XkG1AR89607_NtRr1ef3gNDkZV8UqYsClvX32v6r_38ANr4yw0</recordid><startdate>201211</startdate><enddate>201211</enddate><creator>Reardon, Meaghan</creator><creator>Gobern, Semone</creator><creator>Martinez, Kristina</creator><creator>Shen, Wan</creator><creator>Reid, Tanya</creator><creator>McIntosh, Michael</creator><general>Springer-Verlag</general><general>Springer‐Verlag</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PCBAR</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7S9</scope><scope>L.6</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>201211</creationdate><title>Oleic Acid Attenuates trans-10,cis-12 Conjugated Linoleic Acid-Mediated Inflammatory Gene Expression in Human Adipocytes</title><author>Reardon, Meaghan ; Gobern, Semone ; Martinez, Kristina ; Shen, Wan ; Reid, Tanya ; McIntosh, Michael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5843-1b5441dfe48a9d4b5fd6b03371341b5289b5339e7402349fd1644c9d8a7a452e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adipocytes</topic><topic>Adipocytes - drug effects</topic><topic>Adipocytes - metabolism</topic><topic>Adult</topic><topic>Biomedical and Life Sciences</topic><topic>Cells, Cultured</topic><topic>Conjugated linoleic acid</topic><topic>Dietary Supplements</topic><topic>dose response</topic><topic>Dose-Response Relationship, Drug</topic><topic>Fatty Acids, Monounsaturated - antagonists & inhibitors</topic><topic>Female</topic><topic>G-protein coupled receptors</topic><topic>gene expression</topic><topic>Gene Expression - drug effects</topic><topic>glucose</topic><topic>G‐protein receptors</topic><topic>Humans</topic><topic>inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - genetics</topic><topic>Inflammation - metabolism</topic><topic>Inflammatory gene expression</topic><topic>insulin resistance</topic><topic>isomers</topic><topic>Life Sciences</topic><topic>Linoleic Acids, Conjugated - administration & dosage</topic><topic>Linoleic Acids, Conjugated - pharmacology</topic><topic>lipid content</topic><topic>Lipidology</topic><topic>Medical Biochemistry</topic><topic>Medicinal Chemistry</topic><topic>Microbial Genetics and Genomics</topic><topic>Middle Aged</topic><topic>Monounsaturated fatty acids</topic><topic>Neurochemistry</topic><topic>Nutrition</topic><topic>Oleic acid</topic><topic>Oleic Acids - pharmacology</topic><topic>Original Article</topic><topic>phospholipids</topic><topic>stearic acid</topic><topic>Stearoyl-CoA Desaturase - antagonists & inhibitors</topic><topic>Stearoyl-CoA Desaturase - metabolism</topic><topic>Stearoyl‐CoA desaturase</topic><topic>Structure-Activity Relationship</topic><topic>weight loss</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Reardon, Meaghan</creatorcontrib><creatorcontrib>Gobern, Semone</creatorcontrib><creatorcontrib>Martinez, Kristina</creatorcontrib><creatorcontrib>Shen, Wan</creatorcontrib><creatorcontrib>Reid, Tanya</creatorcontrib><creatorcontrib>McIntosh, Michael</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Earth, Atmospheric & Aquatic Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Earth, Atmospheric & Aquatic Science Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Lipids</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Reardon, Meaghan</au><au>Gobern, Semone</au><au>Martinez, Kristina</au><au>Shen, Wan</au><au>Reid, Tanya</au><au>McIntosh, Michael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oleic Acid Attenuates trans-10,cis-12 Conjugated Linoleic Acid-Mediated Inflammatory Gene Expression in Human Adipocytes</atitle><jtitle>Lipids</jtitle><stitle>Lipids</stitle><addtitle>Lipids</addtitle><date>2012-11</date><risdate>2012</risdate><volume>47</volume><issue>11</issue><spage>1043</spage><epage>1051</epage><pages>1043-1051</pages><issn>0024-4201</issn><eissn>1558-9307</eissn><abstract>The weight loss supplement conjugated linoleic acid (CLA) consists of an equal mixture of
trans
-10,
cis
-12 (10,12) and
cis
-9,
trans
-11 (9,11) isomers. However, high levels of mixed CLA isomers, or the 10,12 isomer, causes chronic inflammation, lipodystrophy, or insulin resistance. We previously demonstrated that 10,12 CLA decreases de novo lipid synthesis along with the abundance and activity of stearoyl-CoA desaturase (SCD)-1, a δ-9 desaturase essential for the synthesis of monounsaturated fatty acids (MUFA). Thus, we hypothesized that the 10,12 CLA-mediated decrease in SCD-1, with the subsequent decrease in MUFA, was responsible for the observed effects. To test this hypothesis, 10,12 CLA-treated human adipocytes were supplemented with oleic acid for 12 h to 7 days, and inflammatory gene expression, insulin-stimulated glucose uptake, and lipid content were measured. Oleic acid reduced inflammatory gene expression in a dose-dependent manner, and restored the lipid content of 10,12 CLA-treated adipocytes without improving insulin-stimulated glucose uptake. In contrast, supplementation with stearic acid, a substrate for SCD-1, or 9,11 CLA did not prevent inflammatory gene expression by 10,12 CLA. Notably, 10,12 CLA impacted the expression of several G-protein coupled receptors that was attenuated by oleic acid. Collectively, these data show that oleic acid attenuates 10,12 CLA-induced inflammatory gene expression and lipid content, possibly by alleviating cell stress caused by the inhibition of MUFA needed for phospholipid and neutral lipid synthesis.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>22941440</pmid><doi>10.1007/s11745-012-3711-0</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adipocytes Adipocytes - drug effects Adipocytes - metabolism Adult Biomedical and Life Sciences Cells, Cultured Conjugated linoleic acid Dietary Supplements dose response Dose-Response Relationship, Drug Fatty Acids, Monounsaturated - antagonists & inhibitors Female G-protein coupled receptors gene expression Gene Expression - drug effects glucose G‐protein receptors Humans inflammation Inflammation - drug therapy Inflammation - genetics Inflammation - metabolism Inflammatory gene expression insulin resistance isomers Life Sciences Linoleic Acids, Conjugated - administration & dosage Linoleic Acids, Conjugated - pharmacology lipid content Lipidology Medical Biochemistry Medicinal Chemistry Microbial Genetics and Genomics Middle Aged Monounsaturated fatty acids Neurochemistry Nutrition Oleic acid Oleic Acids - pharmacology Original Article phospholipids stearic acid Stearoyl-CoA Desaturase - antagonists & inhibitors Stearoyl-CoA Desaturase - metabolism Stearoyl‐CoA desaturase Structure-Activity Relationship weight loss Young Adult |
title | Oleic Acid Attenuates trans-10,cis-12 Conjugated Linoleic Acid-Mediated Inflammatory Gene Expression in Human Adipocytes |
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