Modulation of insulin resistance by PUFA in metabolic tissues
Consumption of polyunsaturated fatty acids (PUFAs) has been shown to be beneficial in the restoration of insulin sensitivity. It has become clear that n‐3 and n‐6 PUFAs act at the nuclear level to affect expression of genes involved in metabolic pathways. PUFAs act via transcription factors such as...
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Veröffentlicht in: | European journal of lipid science and technology 2013-05, Vol.115 (5), p.475-482 |
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creator | Kopal, Martin Muchova, Jana urackova, Zdeka |
description | Consumption of polyunsaturated fatty acids (PUFAs) has been shown to be beneficial in the restoration of insulin sensitivity. It has become clear that n‐3 and n‐6 PUFAs act at the nuclear level to affect expression of genes involved in metabolic pathways. PUFAs act via transcription factors such as PPARs and sterol‐regulatory‐element‐binding proteins (SREBPs) to affect transcription of genes involved in lipogenesis and fatty acid oxidation.
Insulin binds to receptor tyrosin kinase and activates PI‐3K/Akt kinase pathway resulting in incorporation GLUT4 to cell membrane. Insulin also acts via PI‐3K/Akt kinase pathway on the regulation of gene expression. The activation of SREBP‐1c is mediated via PI‐3K and by this way insulin regulate lipid metabolism. ACC – glycerol phosphate acyltransferase, FAS – fatty acid synthase, FOXO – forkhead box protein, PDK1–phosphatidylinositol dependent kinase1, PI‐3K – phosphatidylinositol‐3‐kinase, RTK – receptor tyrosin kinase, SCD1–stearyl‐CoA desaturase‐1. |
doi_str_mv | 10.1002/ejlt.201200229 |
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Insulin binds to receptor tyrosin kinase and activates PI‐3K/Akt kinase pathway resulting in incorporation GLUT4 to cell membrane. Insulin also acts via PI‐3K/Akt kinase pathway on the regulation of gene expression. The activation of SREBP‐1c is mediated via PI‐3K and by this way insulin regulate lipid metabolism. ACC – glycerol phosphate acyltransferase, FAS – fatty acid synthase, FOXO – forkhead box protein, PDK1–phosphatidylinositol dependent kinase1, PI‐3K – phosphatidylinositol‐3‐kinase, RTK – receptor tyrosin kinase, SCD1–stearyl‐CoA desaturase‐1.</description><identifier>ISSN: 1438-7697</identifier><identifier>EISSN: 1438-9312</identifier><identifier>DOI: 10.1002/ejlt.201200229</identifier><language>eng</language><publisher>Weinheim: Blackwell Publishing Ltd</publisher><subject>Fatty acids ; Genes ; Insulin resistance ; Polyunsaturated fatty acids</subject><ispartof>European journal of lipid science and technology, 2013-05, Vol.115 (5), p.475-482</ispartof><rights>2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3559-896df620e227b09fff070abc8ec756ef3054409cac194dbfce29408ec0623d6a3</citedby><cites>FETCH-LOGICAL-c3559-896df620e227b09fff070abc8ec756ef3054409cac194dbfce29408ec0623d6a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fejlt.201200229$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fejlt.201200229$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids></links><search><creatorcontrib>Kopal, Martin</creatorcontrib><creatorcontrib>Muchova, Jana</creatorcontrib><creatorcontrib>urackova, Zdeka</creatorcontrib><title>Modulation of insulin resistance by PUFA in metabolic tissues</title><title>European journal of lipid science and technology</title><addtitle>Eur. J. Lipid Sci. Technol</addtitle><description>Consumption of polyunsaturated fatty acids (PUFAs) has been shown to be beneficial in the restoration of insulin sensitivity. It has become clear that n‐3 and n‐6 PUFAs act at the nuclear level to affect expression of genes involved in metabolic pathways. PUFAs act via transcription factors such as PPARs and sterol‐regulatory‐element‐binding proteins (SREBPs) to affect transcription of genes involved in lipogenesis and fatty acid oxidation.
Insulin binds to receptor tyrosin kinase and activates PI‐3K/Akt kinase pathway resulting in incorporation GLUT4 to cell membrane. Insulin also acts via PI‐3K/Akt kinase pathway on the regulation of gene expression. The activation of SREBP‐1c is mediated via PI‐3K and by this way insulin regulate lipid metabolism. ACC – glycerol phosphate acyltransferase, FAS – fatty acid synthase, FOXO – forkhead box protein, PDK1–phosphatidylinositol dependent kinase1, PI‐3K – phosphatidylinositol‐3‐kinase, RTK – receptor tyrosin kinase, SCD1–stearyl‐CoA desaturase‐1.</description><subject>Fatty acids</subject><subject>Genes</subject><subject>Insulin resistance</subject><subject>Polyunsaturated fatty acids</subject><issn>1438-7697</issn><issn>1438-9312</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNqFkDFPwzAQhS0EEqWwMkdiTrnYiV0PDFVFC1WADq1gsxzHllzSpNiJoP8eV6kqNqa703vfPekhdJvAKAHA93pTtSMMCQ4H5mdokKRkHHOS4PPjzihnl-jK-w0AcEphgB5emrKrZGubOmpMZGvfVbaOnPbWt7JWOir20XI9mwQp2upWFk1lVdRa7zvtr9GFkZXXN8c5ROvZ42r6FOdv8-fpJI8VyTIejzktDcWgMWYFcGMMMJCFGmvFMqoNgSxNgSupEp6WhVEa8xSCChSTkkoyRHf9351rvkJuKzZN5-oQKZIMc8Y4GZPgGvUu5RrvnTZi5-xWur1IQBwqEoeKxKmiAPAe-LaV3v_jFo-LfPWXjXs29KR_Tqx0n4IywjLx_joXbPaxmC9JLnLyCzjOeVc</recordid><startdate>201305</startdate><enddate>201305</enddate><creator>Kopal, Martin</creator><creator>Muchova, Jana</creator><creator>urackova, Zdeka</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>201305</creationdate><title>Modulation of insulin resistance by PUFA in metabolic tissues</title><author>Kopal, Martin ; Muchova, Jana ; urackova, Zdeka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3559-896df620e227b09fff070abc8ec756ef3054409cac194dbfce29408ec0623d6a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Fatty acids</topic><topic>Genes</topic><topic>Insulin resistance</topic><topic>Polyunsaturated fatty acids</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kopal, Martin</creatorcontrib><creatorcontrib>Muchova, Jana</creatorcontrib><creatorcontrib>urackova, Zdeka</creatorcontrib><collection>Istex</collection><collection>CrossRef</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>European journal of lipid science and technology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kopal, Martin</au><au>Muchova, Jana</au><au>urackova, Zdeka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of insulin resistance by PUFA in metabolic tissues</atitle><jtitle>European journal of lipid science and technology</jtitle><addtitle>Eur. J. Lipid Sci. Technol</addtitle><date>2013-05</date><risdate>2013</risdate><volume>115</volume><issue>5</issue><spage>475</spage><epage>482</epage><pages>475-482</pages><issn>1438-7697</issn><eissn>1438-9312</eissn><abstract>Consumption of polyunsaturated fatty acids (PUFAs) has been shown to be beneficial in the restoration of insulin sensitivity. It has become clear that n‐3 and n‐6 PUFAs act at the nuclear level to affect expression of genes involved in metabolic pathways. PUFAs act via transcription factors such as PPARs and sterol‐regulatory‐element‐binding proteins (SREBPs) to affect transcription of genes involved in lipogenesis and fatty acid oxidation.
Insulin binds to receptor tyrosin kinase and activates PI‐3K/Akt kinase pathway resulting in incorporation GLUT4 to cell membrane. Insulin also acts via PI‐3K/Akt kinase pathway on the regulation of gene expression. The activation of SREBP‐1c is mediated via PI‐3K and by this way insulin regulate lipid metabolism. ACC – glycerol phosphate acyltransferase, FAS – fatty acid synthase, FOXO – forkhead box protein, PDK1–phosphatidylinositol dependent kinase1, PI‐3K – phosphatidylinositol‐3‐kinase, RTK – receptor tyrosin kinase, SCD1–stearyl‐CoA desaturase‐1.</abstract><cop>Weinheim</cop><pub>Blackwell Publishing Ltd</pub><doi>10.1002/ejlt.201200229</doi><tpages>8</tpages></addata></record> |
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subjects | Fatty acids Genes Insulin resistance Polyunsaturated fatty acids |
title | Modulation of insulin resistance by PUFA in metabolic tissues |
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