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Oleate dose-dependently regulates palmitate metabolism and insulin signaling in C2C12 myotubes
Because the protective effect of oleate against palmitate-induced insulin resistance may be lessened in skeletal muscle once cell metabolism is overloaded by fatty acids (FAs), we examined the impact of varying amounts of oleate on palmitate metabolic channeling and insulin signaling in C2C12 myotub...
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| Published in: | Biochimica et biophysica acta 2016-12, Vol.1861 (12), p.2000-2010 |
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| cites | cdi_FETCH-LOGICAL-c396t-2e053da58d22490713913fc224f6128178fb454aebc8cce9e10289bbe77330783 |
| container_end_page | 2010 |
| container_issue | 12 |
| container_start_page | 2000 |
| container_title | Biochimica et biophysica acta |
| container_volume | 1861 |
| creator | Capel, Frédéric Cheraiti, Naoufel Acquaviva, Cécile Hénique, Carole Bertrand-Michel, Justine Vianey-Saban, Christine Prip-Buus, Carina Morio, Béatrice |
| description | Because the protective effect of oleate against palmitate-induced insulin resistance may be lessened in skeletal muscle once cell metabolism is overloaded by fatty acids (FAs), we examined the impact of varying amounts of oleate on palmitate metabolic channeling and insulin signaling in C2C12 myotubes. Cells were exposed to 0.5mM of palmitate and to increasing doses of oleate (0.05, 0.25 and 0.5mM). Impacts of FA treatments on radio-labelled FA fluxes, on cellular content in diacylglycerols (DAG), triacylglycerols (TAG), ceramides, acylcarnitines, on PKCθ, MAPKs (ERK1/2, p38) and NF-ΚB activation, and on insulin-dependent Akt phosphorylation were examined.
Low dose of oleate (0.05mM) was sufficient to improve palmitate complete oxidation to CO2 (+29%, P |
| doi_str_mv | 10.1016/j.bbalip.2016.10.002 |
| format | article |
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Low dose of oleate (0.05mM) was sufficient to improve palmitate complete oxidation to CO2 (+29%, P<0.05) and to alter the cellular acylcarnitine profile. Insulin-induced Akt phosphorylation was 48% higher in that condition vs. palmitate alone (p<0.01). Although DAG and ceramide contents were significantly decreased with 0.05mM of oleate vs. palmitate alone (−47 and −28%, respectively, p<0.01), 0.25mM of oleate was required to decrease p38 MAPK and PKCθ phosphorylation, thus further improving the insulin signaling (+32%, p<0.05). By contrast, increasing oleate concentration from 0.25 to 0.5mM, thus increasing total amount of FA from 0.75 to 1mM, deteriorated the insulin signaling pathway (−30%, p<0.01). This was observed despite low contents in DAG and ceramides, and enhanced palmitate incorporation into TAG (+27%, p<0.05). This was associated with increased incomplete FA β-oxidation and impairment of acylcarnitine profile. In conclusion, these combined data place mitochondrial β-oxidation at the center of the regulation of muscle insulin sensitivity, besides p38 MAPK and PKCθ.
•Oleate significantly alters palmitate channeling in C2C12 myotubes.•Impact of oleate on palmitate-induced insulin resistance follows an inverted U-curve.•Low dose of oleate is sufficient to enhance palmitate complete oxidation to CO2.•Dual effect of oleate on insulin signaling involves improved β-oxidation and inhibition of PKCθ and p38 MAPK.•Oleate overload increases incomplete β-oxidation and alters insulin signaling.]]></description><identifier>ISSN: 1388-1981</identifier><identifier>ISSN: 0006-3002</identifier><identifier>EISSN: 1879-2618</identifier><identifier>DOI: 10.1016/j.bbalip.2016.10.002</identifier><identifier>PMID: 27725263</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Carnitine - analogs & derivatives ; Carnitine - metabolism ; Cell Line ; Ceramides - metabolism ; Diglycerides - metabolism ; Fatty Acids - metabolism ; Food and Nutrition ; Insulin - metabolism ; Insulin Resistance - physiology ; Insulin signaling ; Life Sciences ; Lipid metabolism ; Lipotoxicity ; Mice ; Muscle Fibers, Skeletal - drug effects ; Muscle Fibers, Skeletal - metabolism ; Muscle, Skeletal - drug effects ; Muscle, Skeletal - metabolism ; NF-kappa B - metabolism ; Oleic Acid - pharmacology ; Oxidation-Reduction - drug effects ; p38 Mitogen-Activated Protein Kinases - metabolism ; Palmitates - metabolism ; Phosphorylation - drug effects ; Phosphorylation - physiology ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Skeletal muscle ; Substrate partitioning ; Triglycerides - metabolism</subject><ispartof>Biochimica et biophysica acta, 2016-12, Vol.1861 (12), p.2000-2010</ispartof><rights>2016 Elsevier B.V.</rights><rights>Copyright © 2016 Elsevier B.V. All rights reserved.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-2e053da58d22490713913fc224f6128178fb454aebc8cce9e10289bbe77330783</citedby><cites>FETCH-LOGICAL-c396t-2e053da58d22490713913fc224f6128178fb454aebc8cce9e10289bbe77330783</cites><orcidid>0000-0002-3828-6847 ; 0000-0002-2418-1438 ; 0000-0002-0133-0277</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27725263$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-01594528$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Capel, Frédéric</creatorcontrib><creatorcontrib>Cheraiti, Naoufel</creatorcontrib><creatorcontrib>Acquaviva, Cécile</creatorcontrib><creatorcontrib>Hénique, Carole</creatorcontrib><creatorcontrib>Bertrand-Michel, Justine</creatorcontrib><creatorcontrib>Vianey-Saban, Christine</creatorcontrib><creatorcontrib>Prip-Buus, Carina</creatorcontrib><creatorcontrib>Morio, Béatrice</creatorcontrib><title>Oleate dose-dependently regulates palmitate metabolism and insulin signaling in C2C12 myotubes</title><title>Biochimica et biophysica acta</title><addtitle>Biochim Biophys Acta</addtitle><description><![CDATA[Because the protective effect of oleate against palmitate-induced insulin resistance may be lessened in skeletal muscle once cell metabolism is overloaded by fatty acids (FAs), we examined the impact of varying amounts of oleate on palmitate metabolic channeling and insulin signaling in C2C12 myotubes. Cells were exposed to 0.5mM of palmitate and to increasing doses of oleate (0.05, 0.25 and 0.5mM). Impacts of FA treatments on radio-labelled FA fluxes, on cellular content in diacylglycerols (DAG), triacylglycerols (TAG), ceramides, acylcarnitines, on PKCθ, MAPKs (ERK1/2, p38) and NF-ΚB activation, and on insulin-dependent Akt phosphorylation were examined.
Low dose of oleate (0.05mM) was sufficient to improve palmitate complete oxidation to CO2 (+29%, P<0.05) and to alter the cellular acylcarnitine profile. Insulin-induced Akt phosphorylation was 48% higher in that condition vs. palmitate alone (p<0.01). Although DAG and ceramide contents were significantly decreased with 0.05mM of oleate vs. palmitate alone (−47 and −28%, respectively, p<0.01), 0.25mM of oleate was required to decrease p38 MAPK and PKCθ phosphorylation, thus further improving the insulin signaling (+32%, p<0.05). By contrast, increasing oleate concentration from 0.25 to 0.5mM, thus increasing total amount of FA from 0.75 to 1mM, deteriorated the insulin signaling pathway (−30%, p<0.01). This was observed despite low contents in DAG and ceramides, and enhanced palmitate incorporation into TAG (+27%, p<0.05). This was associated with increased incomplete FA β-oxidation and impairment of acylcarnitine profile. In conclusion, these combined data place mitochondrial β-oxidation at the center of the regulation of muscle insulin sensitivity, besides p38 MAPK and PKCθ.
•Oleate significantly alters palmitate channeling in C2C12 myotubes.•Impact of oleate on palmitate-induced insulin resistance follows an inverted U-curve.•Low dose of oleate is sufficient to enhance palmitate complete oxidation to CO2.•Dual effect of oleate on insulin signaling involves improved β-oxidation and inhibition of PKCθ and p38 MAPK.•Oleate overload increases incomplete β-oxidation and alters insulin signaling.]]></description><subject>Animals</subject><subject>Carnitine - analogs & derivatives</subject><subject>Carnitine - metabolism</subject><subject>Cell Line</subject><subject>Ceramides - metabolism</subject><subject>Diglycerides - metabolism</subject><subject>Fatty Acids - metabolism</subject><subject>Food and Nutrition</subject><subject>Insulin - metabolism</subject><subject>Insulin Resistance - physiology</subject><subject>Insulin signaling</subject><subject>Life Sciences</subject><subject>Lipid metabolism</subject><subject>Lipotoxicity</subject><subject>Mice</subject><subject>Muscle Fibers, Skeletal - drug effects</subject><subject>Muscle Fibers, Skeletal - metabolism</subject><subject>Muscle, Skeletal - drug effects</subject><subject>Muscle, Skeletal - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Oleic Acid - pharmacology</subject><subject>Oxidation-Reduction - drug effects</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Palmitates - metabolism</subject><subject>Phosphorylation - drug effects</subject><subject>Phosphorylation - physiology</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Skeletal muscle</subject><subject>Substrate partitioning</subject><subject>Triglycerides - metabolism</subject><issn>1388-1981</issn><issn>0006-3002</issn><issn>1879-2618</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNp9kctu1DAUhi1E1ZbSN0AoS1hk8LFzsTdI1ahQpJG6gS2WLyeDR44T4qTSvH0dpXTJyj6_v3Px-Qn5AHQHFJovp50xOvhxx3KUpR2l7A25BtHKkjUg3uY7F6IEKeCKvEvpRCnUnNeX5Iq1LatZw6_J78eAesbCDQlLhyNGh3EO52LC4xLySypGHXo_r1CPszZD8KkvdHSFj2kJPhbJH2OeJB6zUuzZHljRn4d5MZjek4tOh4S3L-cN-fXt_uf-oTw8fv-xvzuUlstmLhnSmjtdC8dYJWkLXALvbA66BpiAVnSmqiuNxgprUSJQJqQx2Lac01bwG_J5q_tHBzVOvtfTWQ3aq4e7g1q1_HVZ1Uw8QWY_bew4DX8XTLPqfbIYgo44LEmB4DWXeYUyo9WG2mlIacLutTZQtbqgTmpzQa0urGp2Iad9fOmwmB7da9K_tWfg6wZg3smTx0kl6zFadH5COys3-P93eAZGRZkP</recordid><startdate>20161201</startdate><enddate>20161201</enddate><creator>Capel, Frédéric</creator><creator>Cheraiti, Naoufel</creator><creator>Acquaviva, Cécile</creator><creator>Hénique, Carole</creator><creator>Bertrand-Michel, Justine</creator><creator>Vianey-Saban, Christine</creator><creator>Prip-Buus, Carina</creator><creator>Morio, Béatrice</creator><general>Elsevier B.V</general><general>Elsevier</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>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-3828-6847</orcidid><orcidid>https://orcid.org/0000-0002-2418-1438</orcidid><orcidid>https://orcid.org/0000-0002-0133-0277</orcidid></search><sort><creationdate>20161201</creationdate><title>Oleate dose-dependently regulates palmitate metabolism and insulin signaling in C2C12 myotubes</title><author>Capel, Frédéric ; Cheraiti, Naoufel ; Acquaviva, Cécile ; Hénique, Carole ; Bertrand-Michel, Justine ; Vianey-Saban, Christine ; Prip-Buus, Carina ; Morio, Béatrice</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-2e053da58d22490713913fc224f6128178fb454aebc8cce9e10289bbe77330783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Carnitine - analogs & derivatives</topic><topic>Carnitine - metabolism</topic><topic>Cell Line</topic><topic>Ceramides - metabolism</topic><topic>Diglycerides - metabolism</topic><topic>Fatty Acids - metabolism</topic><topic>Food and Nutrition</topic><topic>Insulin - metabolism</topic><topic>Insulin Resistance - physiology</topic><topic>Insulin signaling</topic><topic>Life Sciences</topic><topic>Lipid metabolism</topic><topic>Lipotoxicity</topic><topic>Mice</topic><topic>Muscle Fibers, Skeletal - drug effects</topic><topic>Muscle Fibers, Skeletal - metabolism</topic><topic>Muscle, Skeletal - drug effects</topic><topic>Muscle, Skeletal - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Oleic Acid - pharmacology</topic><topic>Oxidation-Reduction - drug effects</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Palmitates - metabolism</topic><topic>Phosphorylation - drug effects</topic><topic>Phosphorylation - physiology</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Skeletal muscle</topic><topic>Substrate partitioning</topic><topic>Triglycerides - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Capel, Frédéric</creatorcontrib><creatorcontrib>Cheraiti, Naoufel</creatorcontrib><creatorcontrib>Acquaviva, Cécile</creatorcontrib><creatorcontrib>Hénique, Carole</creatorcontrib><creatorcontrib>Bertrand-Michel, Justine</creatorcontrib><creatorcontrib>Vianey-Saban, Christine</creatorcontrib><creatorcontrib>Prip-Buus, Carina</creatorcontrib><creatorcontrib>Morio, Béatrice</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Biochimica et biophysica acta</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Capel, Frédéric</au><au>Cheraiti, Naoufel</au><au>Acquaviva, Cécile</au><au>Hénique, Carole</au><au>Bertrand-Michel, Justine</au><au>Vianey-Saban, Christine</au><au>Prip-Buus, Carina</au><au>Morio, Béatrice</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oleate dose-dependently regulates palmitate metabolism and insulin signaling in C2C12 myotubes</atitle><jtitle>Biochimica et biophysica acta</jtitle><addtitle>Biochim Biophys Acta</addtitle><date>2016-12-01</date><risdate>2016</risdate><volume>1861</volume><issue>12</issue><spage>2000</spage><epage>2010</epage><pages>2000-2010</pages><issn>1388-1981</issn><issn>0006-3002</issn><eissn>1879-2618</eissn><abstract><![CDATA[Because the protective effect of oleate against palmitate-induced insulin resistance may be lessened in skeletal muscle once cell metabolism is overloaded by fatty acids (FAs), we examined the impact of varying amounts of oleate on palmitate metabolic channeling and insulin signaling in C2C12 myotubes. Cells were exposed to 0.5mM of palmitate and to increasing doses of oleate (0.05, 0.25 and 0.5mM). Impacts of FA treatments on radio-labelled FA fluxes, on cellular content in diacylglycerols (DAG), triacylglycerols (TAG), ceramides, acylcarnitines, on PKCθ, MAPKs (ERK1/2, p38) and NF-ΚB activation, and on insulin-dependent Akt phosphorylation were examined.
Low dose of oleate (0.05mM) was sufficient to improve palmitate complete oxidation to CO2 (+29%, P<0.05) and to alter the cellular acylcarnitine profile. Insulin-induced Akt phosphorylation was 48% higher in that condition vs. palmitate alone (p<0.01). Although DAG and ceramide contents were significantly decreased with 0.05mM of oleate vs. palmitate alone (−47 and −28%, respectively, p<0.01), 0.25mM of oleate was required to decrease p38 MAPK and PKCθ phosphorylation, thus further improving the insulin signaling (+32%, p<0.05). By contrast, increasing oleate concentration from 0.25 to 0.5mM, thus increasing total amount of FA from 0.75 to 1mM, deteriorated the insulin signaling pathway (−30%, p<0.01). This was observed despite low contents in DAG and ceramides, and enhanced palmitate incorporation into TAG (+27%, p<0.05). This was associated with increased incomplete FA β-oxidation and impairment of acylcarnitine profile. In conclusion, these combined data place mitochondrial β-oxidation at the center of the regulation of muscle insulin sensitivity, besides p38 MAPK and PKCθ.
•Oleate significantly alters palmitate channeling in C2C12 myotubes.•Impact of oleate on palmitate-induced insulin resistance follows an inverted U-curve.•Low dose of oleate is sufficient to enhance palmitate complete oxidation to CO2.•Dual effect of oleate on insulin signaling involves improved β-oxidation and inhibition of PKCθ and p38 MAPK.•Oleate overload increases incomplete β-oxidation and alters insulin signaling.]]></abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>27725263</pmid><doi>10.1016/j.bbalip.2016.10.002</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-3828-6847</orcidid><orcidid>https://orcid.org/0000-0002-2418-1438</orcidid><orcidid>https://orcid.org/0000-0002-0133-0277</orcidid></addata></record> |
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| ispartof | Biochimica et biophysica acta, 2016-12, Vol.1861 (12), p.2000-2010 |
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| source | Elsevier |
| subjects | Animals Carnitine - analogs & derivatives Carnitine - metabolism Cell Line Ceramides - metabolism Diglycerides - metabolism Fatty Acids - metabolism Food and Nutrition Insulin - metabolism Insulin Resistance - physiology Insulin signaling Life Sciences Lipid metabolism Lipotoxicity Mice Muscle Fibers, Skeletal - drug effects Muscle Fibers, Skeletal - metabolism Muscle, Skeletal - drug effects Muscle, Skeletal - metabolism NF-kappa B - metabolism Oleic Acid - pharmacology Oxidation-Reduction - drug effects p38 Mitogen-Activated Protein Kinases - metabolism Palmitates - metabolism Phosphorylation - drug effects Phosphorylation - physiology Proto-Oncogene Proteins c-akt - metabolism Signal Transduction - drug effects Signal Transduction - physiology Skeletal muscle Substrate partitioning Triglycerides - metabolism |
| title | Oleate dose-dependently regulates palmitate metabolism and insulin signaling in C2C12 myotubes |
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