The role of the Nrf2/Keap1 pathway in obesity and metabolic syndrome
Nuclear factor erythroid 2 related factor 2 (Nrf2) is a key regulator of antioxidant signaling that may prevent the development of metabolic syndrome and related cardiovascular diseases. However, emerging evidence shows that lack of Nrf2 could ameliorate insulin resistance, adipogenesis and adipocyt...
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Veröffentlicht in: | Reviews in endocrine & metabolic disorders 2015-03, Vol.16 (1), p.35-45 |
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description | Nuclear factor erythroid 2 related factor 2 (Nrf2) is a key regulator of antioxidant signaling that may prevent the development of metabolic syndrome and related cardiovascular diseases. However, emerging evidence shows that lack of Nrf2 could ameliorate insulin resistance, adipogenesis and adipocyte differentiation. Consistent with this, overexpression of Nrf2 gene could also cause insulin resistance under certain conditions. Furthermore, an increasing number of studies indicate that redox balance can be a critical element that contributes to the contradictory effects of Nrf2 on insulin sensitivity and resistance. Reactive oxygen species can promote normal insulin-mediated signal transduction under physiological conditions but also induce insulin resistance under certain pathological conditions. Therefore, the contradictory effects of Nrf2 on insulin signaling pathways may be related to its regulation of redox homeostasis. This review attempts to summarize the latest developments in our understanding of the mechanisms of Nrf2-mediated signaling and its role in the modulation of metabolic homeostasis. |
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However, emerging evidence shows that lack of Nrf2 could ameliorate insulin resistance, adipogenesis and adipocyte differentiation. Consistent with this, overexpression of Nrf2 gene could also cause insulin resistance under certain conditions. Furthermore, an increasing number of studies indicate that redox balance can be a critical element that contributes to the contradictory effects of Nrf2 on insulin sensitivity and resistance. Reactive oxygen species can promote normal insulin-mediated signal transduction under physiological conditions but also induce insulin resistance under certain pathological conditions. Therefore, the contradictory effects of Nrf2 on insulin signaling pathways may be related to its regulation of redox homeostasis. This review attempts to summarize the latest developments in our understanding of the mechanisms of Nrf2-mediated signaling and its role in the modulation of metabolic homeostasis.</description><identifier>ISSN: 1389-9155</identifier><identifier>EISSN: 1573-2606</identifier><identifier>DOI: 10.1007/s11154-014-9305-9</identifier><identifier>PMID: 25540093</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Diabetes ; Endocrinology ; Homeostasis - physiology ; Humans ; Insulin Resistance - physiology ; Internal Medicine ; Intracellular Signaling Peptides and Proteins - metabolism ; Kelch-Like ECH-Associated Protein 1 ; Medicine ; Medicine & Public Health ; Metabolic Syndrome - metabolism ; NF-E2-Related Factor 2 - metabolism ; Obesity - metabolism ; Reactive Oxygen Species - metabolism ; Signal Transduction - physiology</subject><ispartof>Reviews in endocrine & metabolic disorders, 2015-03, Vol.16 (1), p.35-45</ispartof><rights>Springer Science+Business Media New York 2014</rights><rights>Springer Science+Business Media New York 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c541t-20b56a0a69b47deb82a0b3e1d157996d41006ff48ffaee62e9e0e26dde29647d3</citedby><cites>FETCH-LOGICAL-c541t-20b56a0a69b47deb82a0b3e1d157996d41006ff48ffaee62e9e0e26dde29647d3</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/s11154-014-9305-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11154-014-9305-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25540093$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Zhiguo</creatorcontrib><creatorcontrib>Zhou, Shanshan</creatorcontrib><creatorcontrib>Jiang, Xin</creatorcontrib><creatorcontrib>Wang, Yue-Hui</creatorcontrib><creatorcontrib>Li, Fengsheng</creatorcontrib><creatorcontrib>Wang, Yong-Gang</creatorcontrib><creatorcontrib>Zheng, Yang</creatorcontrib><creatorcontrib>Cai, Lu</creatorcontrib><title>The role of the Nrf2/Keap1 pathway in obesity and metabolic syndrome</title><title>Reviews in endocrine & metabolic disorders</title><addtitle>Rev Endocr Metab Disord</addtitle><addtitle>Rev Endocr Metab Disord</addtitle><description>Nuclear factor erythroid 2 related factor 2 (Nrf2) is a key regulator of antioxidant signaling that may prevent the development of metabolic syndrome and related cardiovascular diseases. 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This review attempts to summarize the latest developments in our understanding of the mechanisms of Nrf2-mediated signaling and its role in the modulation of metabolic homeostasis.</description><subject>Diabetes</subject><subject>Endocrinology</subject><subject>Homeostasis - physiology</subject><subject>Humans</subject><subject>Insulin Resistance - physiology</subject><subject>Internal Medicine</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Kelch-Like ECH-Associated Protein 1</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Syndrome - metabolism</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Obesity - metabolism</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction - physiology</subject><issn>1389-9155</issn><issn>1573-2606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkU9LxDAQxYMo7rr6AbxIwIuX6iRt0uYo619c9LKeQ7qdul3aZk26SL-9WbqKCOIlGZjfe8nMI-SUwSUDSK88Y0wkEbAkUjGISO2RMRNpHHEJcj_UcaYixYQYkSPvVwCcSSUOyYgLkQCoeExu5kukztZIbUm7UD-7kl89oVkzujbd8sP0tGqpzdFXXU9NW9AGO5PbulpQ37eFsw0ek4PS1B5PdveEvN7dzqcP0ezl_nF6PYsWImFdxCEX0oCRKk_SAvOMG8hjZEX4s1KySMJQsiyTrCwNouSoEJDLokCuZFDEE3Ix-K6dfd-g73RT-QXWtWnRbrxmmUrjVITjf1RKSOJUsS16_gtd2Y1rwyCBEpniIKQKFBuohbPeOyz12lWNcb1moLdp6CENHdLQ2zT0VnO2c97kDRbfiq_1B4APgA-t9g3dj6f_dP0E_KeSSw</recordid><startdate>20150301</startdate><enddate>20150301</enddate><creator>Zhang, Zhiguo</creator><creator>Zhou, Shanshan</creator><creator>Jiang, Xin</creator><creator>Wang, Yue-Hui</creator><creator>Li, Fengsheng</creator><creator>Wang, Yong-Gang</creator><creator>Zheng, Yang</creator><creator>Cai, Lu</creator><general>Springer US</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7TS</scope></search><sort><creationdate>20150301</creationdate><title>The role of the Nrf2/Keap1 pathway in obesity and metabolic syndrome</title><author>Zhang, Zhiguo ; Zhou, Shanshan ; Jiang, Xin ; Wang, Yue-Hui ; Li, Fengsheng ; Wang, Yong-Gang ; Zheng, Yang ; Cai, Lu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c541t-20b56a0a69b47deb82a0b3e1d157996d41006ff48ffaee62e9e0e26dde29647d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Diabetes</topic><topic>Endocrinology</topic><topic>Homeostasis - physiology</topic><topic>Humans</topic><topic>Insulin Resistance - physiology</topic><topic>Internal Medicine</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Kelch-Like ECH-Associated Protein 1</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Syndrome - metabolism</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Obesity - metabolism</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Zhiguo</creatorcontrib><creatorcontrib>Zhou, Shanshan</creatorcontrib><creatorcontrib>Jiang, Xin</creatorcontrib><creatorcontrib>Wang, Yue-Hui</creatorcontrib><creatorcontrib>Li, Fengsheng</creatorcontrib><creatorcontrib>Wang, Yong-Gang</creatorcontrib><creatorcontrib>Zheng, Yang</creatorcontrib><creatorcontrib>Cai, Lu</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Physical Education Index</collection><jtitle>Reviews in endocrine & metabolic disorders</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Zhiguo</au><au>Zhou, Shanshan</au><au>Jiang, Xin</au><au>Wang, Yue-Hui</au><au>Li, Fengsheng</au><au>Wang, Yong-Gang</au><au>Zheng, Yang</au><au>Cai, Lu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of the Nrf2/Keap1 pathway in obesity and metabolic syndrome</atitle><jtitle>Reviews in endocrine & metabolic disorders</jtitle><stitle>Rev Endocr Metab Disord</stitle><addtitle>Rev Endocr Metab Disord</addtitle><date>2015-03-01</date><risdate>2015</risdate><volume>16</volume><issue>1</issue><spage>35</spage><epage>45</epage><pages>35-45</pages><issn>1389-9155</issn><eissn>1573-2606</eissn><abstract>Nuclear factor erythroid 2 related factor 2 (Nrf2) is a key regulator of antioxidant signaling that may prevent the development of metabolic syndrome and related cardiovascular diseases. However, emerging evidence shows that lack of Nrf2 could ameliorate insulin resistance, adipogenesis and adipocyte differentiation. Consistent with this, overexpression of Nrf2 gene could also cause insulin resistance under certain conditions. Furthermore, an increasing number of studies indicate that redox balance can be a critical element that contributes to the contradictory effects of Nrf2 on insulin sensitivity and resistance. Reactive oxygen species can promote normal insulin-mediated signal transduction under physiological conditions but also induce insulin resistance under certain pathological conditions. Therefore, the contradictory effects of Nrf2 on insulin signaling pathways may be related to its regulation of redox homeostasis. 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subjects | Diabetes Endocrinology Homeostasis - physiology Humans Insulin Resistance - physiology Internal Medicine Intracellular Signaling Peptides and Proteins - metabolism Kelch-Like ECH-Associated Protein 1 Medicine Medicine & Public Health Metabolic Syndrome - metabolism NF-E2-Related Factor 2 - metabolism Obesity - metabolism Reactive Oxygen Species - metabolism Signal Transduction - physiology |
title | The role of the Nrf2/Keap1 pathway in obesity and metabolic syndrome |
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