KPNβ1 promotes palmitate-induced insulin resistance via NF-κB signaling in hepatocytes
It has been intensively studied that inflammation contributes to the insulin resistance development in obesity-induced type 2 diabetes mellitus (T2DM). In this study, we assessed the effect of karyopherin β1 (KPNβ1) in hepatic insulin resistance and the underlying mechanisms using high-fat diet (HFD...
Gespeichert in:
| Veröffentlicht in: | Journal of physiology and biochemistry 2015-12, Vol.71 (4), p.763-772 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 772 |
|---|---|
| container_issue | 4 |
| container_start_page | 763 |
| container_title | Journal of physiology and biochemistry |
| container_volume | 71 |
| creator | Wang, Suxin Zhao, Yun Xia, Nana Zhang, Wanlu Tang, Zhuqi Wang, Cuifang Zhu, Xiaohui Cui, Shiwei |
| description | It has been intensively studied that inflammation contributes to the insulin resistance development in obesity-induced type 2 diabetes mellitus (T2DM). In this study, we assessed the effect of karyopherin β1 (KPNβ1) in hepatic insulin resistance and the underlying mechanisms using high-fat diet (HFD) fed mice and palmitate (PA)-stimulated hepatocytes (HepG2). KPNβ1 expression is increased in the HFD fed mice liver. PA upregulated KPNβ1 expression in HepG2 cells in a time-dependent manner. PA also increased pro-inflammatory cytokines expression, including tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and interleukin 1β (IL-1β). KPNβ1 knockdown reversed PA-induced pro-inflammatory cytokines expression and insulin-stimulated glucose uptake in HepG2 cells. In addition, KPNβ1 knockdown reduced intracellular lipid accumulation. Mechanistically, KPNβ1 transports nuclear factor kB (NF-κB) p65 from the cytoplasm to the nucleus to increase pro-inflammatory genes expression. In summary, KPNβ1 acts as a positive regulator in the NF-κB pathway to enhance palmitate-induced inflammation response and insulin resistance in HepG2 cells. |
| doi_str_mv | 10.1007/s13105-015-0440-x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1744662810</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1744662810</sourcerecordid><originalsourceid>FETCH-LOGICAL-c329x-d88b46606d70472c5ec366b4609a9ed2e041a6339c7f4c327633f1cbca93a27e3</originalsourceid><addsrcrecordid>eNp9kLtOwzAUhi0EoqXwACzII4vBt8TJCBUFRFUYQGKzXOekuMqlxAlqX4uRh-gz4SrAyGD5yOf_P8kfQqeMXjBK1aVngtGIUBaOlJSs99CQJUqRREXRfpiZSIiKZDJAR94vKZWccXqIBjyWEY8oG6LXh6fZ9pPhVVOXdQser0xRuta0QFyVdRYy7CrfFa7CDXjnW1NZwB_O4NmEbL-usXeLyoT1IuTwG6xMW9tNAB2jg9wUHk5-7hF6mdw8j-_I9PH2fnw1JVbwdE2yJJnLOKZxpqhU3EZgRRyHJ5qaFDIOVDITC5FalctQUWHOmZ1bkwrDFYgROu-54QfvHfhWl85bKApTQd15zZQMfJ4wGqKsj9qm9r6BXK8aV5pmoxnVO6G6F6qDUL0Tqtehc_aD7-YlZH-NX4MhwPuAD6tqAY1e1l0TlPh_qN9C3oJi</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1744662810</pqid></control><display><type>article</type><title>KPNβ1 promotes palmitate-induced insulin resistance via NF-κB signaling in hepatocytes</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Wang, Suxin ; Zhao, Yun ; Xia, Nana ; Zhang, Wanlu ; Tang, Zhuqi ; Wang, Cuifang ; Zhu, Xiaohui ; Cui, Shiwei</creator><creatorcontrib>Wang, Suxin ; Zhao, Yun ; Xia, Nana ; Zhang, Wanlu ; Tang, Zhuqi ; Wang, Cuifang ; Zhu, Xiaohui ; Cui, Shiwei</creatorcontrib><description>It has been intensively studied that inflammation contributes to the insulin resistance development in obesity-induced type 2 diabetes mellitus (T2DM). In this study, we assessed the effect of karyopherin β1 (KPNβ1) in hepatic insulin resistance and the underlying mechanisms using high-fat diet (HFD) fed mice and palmitate (PA)-stimulated hepatocytes (HepG2). KPNβ1 expression is increased in the HFD fed mice liver. PA upregulated KPNβ1 expression in HepG2 cells in a time-dependent manner. PA also increased pro-inflammatory cytokines expression, including tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and interleukin 1β (IL-1β). KPNβ1 knockdown reversed PA-induced pro-inflammatory cytokines expression and insulin-stimulated glucose uptake in HepG2 cells. In addition, KPNβ1 knockdown reduced intracellular lipid accumulation. Mechanistically, KPNβ1 transports nuclear factor kB (NF-κB) p65 from the cytoplasm to the nucleus to increase pro-inflammatory genes expression. In summary, KPNβ1 acts as a positive regulator in the NF-κB pathway to enhance palmitate-induced inflammation response and insulin resistance in HepG2 cells.</description><identifier>ISSN: 1138-7548</identifier><identifier>EISSN: 1877-8755</identifier><identifier>DOI: 10.1007/s13105-015-0440-x</identifier><identifier>PMID: 26452501</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Active Transport, Cell Nucleus ; Animal Physiology ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Hep G2 Cells ; Hepatocytes - metabolism ; Human Physiology ; Humans ; Insulin - physiology ; Insulin Resistance ; Liver - metabolism ; Liver - pathology ; Male ; Mice, Inbred C57BL ; Nuclear Proteins - physiology ; Original Paper ; Palmitates ; Signal Transduction ; Transcription Factor RelA - metabolism</subject><ispartof>Journal of physiology and biochemistry, 2015-12, Vol.71 (4), p.763-772</ispartof><rights>University of Navarra 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c329x-d88b46606d70472c5ec366b4609a9ed2e041a6339c7f4c327633f1cbca93a27e3</citedby><cites>FETCH-LOGICAL-c329x-d88b46606d70472c5ec366b4609a9ed2e041a6339c7f4c327633f1cbca93a27e3</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/s13105-015-0440-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s13105-015-0440-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26452501$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Suxin</creatorcontrib><creatorcontrib>Zhao, Yun</creatorcontrib><creatorcontrib>Xia, Nana</creatorcontrib><creatorcontrib>Zhang, Wanlu</creatorcontrib><creatorcontrib>Tang, Zhuqi</creatorcontrib><creatorcontrib>Wang, Cuifang</creatorcontrib><creatorcontrib>Zhu, Xiaohui</creatorcontrib><creatorcontrib>Cui, Shiwei</creatorcontrib><title>KPNβ1 promotes palmitate-induced insulin resistance via NF-κB signaling in hepatocytes</title><title>Journal of physiology and biochemistry</title><addtitle>J Physiol Biochem</addtitle><addtitle>J Physiol Biochem</addtitle><description>It has been intensively studied that inflammation contributes to the insulin resistance development in obesity-induced type 2 diabetes mellitus (T2DM). In this study, we assessed the effect of karyopherin β1 (KPNβ1) in hepatic insulin resistance and the underlying mechanisms using high-fat diet (HFD) fed mice and palmitate (PA)-stimulated hepatocytes (HepG2). KPNβ1 expression is increased in the HFD fed mice liver. PA upregulated KPNβ1 expression in HepG2 cells in a time-dependent manner. PA also increased pro-inflammatory cytokines expression, including tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and interleukin 1β (IL-1β). KPNβ1 knockdown reversed PA-induced pro-inflammatory cytokines expression and insulin-stimulated glucose uptake in HepG2 cells. In addition, KPNβ1 knockdown reduced intracellular lipid accumulation. Mechanistically, KPNβ1 transports nuclear factor kB (NF-κB) p65 from the cytoplasm to the nucleus to increase pro-inflammatory genes expression. In summary, KPNβ1 acts as a positive regulator in the NF-κB pathway to enhance palmitate-induced inflammation response and insulin resistance in HepG2 cells.</description><subject>Active Transport, Cell Nucleus</subject><subject>Animal Physiology</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Hep G2 Cells</subject><subject>Hepatocytes - metabolism</subject><subject>Human Physiology</subject><subject>Humans</subject><subject>Insulin - physiology</subject><subject>Insulin Resistance</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Male</subject><subject>Mice, Inbred C57BL</subject><subject>Nuclear Proteins - physiology</subject><subject>Original Paper</subject><subject>Palmitates</subject><subject>Signal Transduction</subject><subject>Transcription Factor RelA - metabolism</subject><issn>1138-7548</issn><issn>1877-8755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kLtOwzAUhi0EoqXwACzII4vBt8TJCBUFRFUYQGKzXOekuMqlxAlqX4uRh-gz4SrAyGD5yOf_P8kfQqeMXjBK1aVngtGIUBaOlJSs99CQJUqRREXRfpiZSIiKZDJAR94vKZWccXqIBjyWEY8oG6LXh6fZ9pPhVVOXdQser0xRuta0QFyVdRYy7CrfFa7CDXjnW1NZwB_O4NmEbL-usXeLyoT1IuTwG6xMW9tNAB2jg9wUHk5-7hF6mdw8j-_I9PH2fnw1JVbwdE2yJJnLOKZxpqhU3EZgRRyHJ5qaFDIOVDITC5FalctQUWHOmZ1bkwrDFYgROu-54QfvHfhWl85bKApTQd15zZQMfJ4wGqKsj9qm9r6BXK8aV5pmoxnVO6G6F6qDUL0Tqtehc_aD7-YlZH-NX4MhwPuAD6tqAY1e1l0TlPh_qN9C3oJi</recordid><startdate>20151201</startdate><enddate>20151201</enddate><creator>Wang, Suxin</creator><creator>Zhao, Yun</creator><creator>Xia, Nana</creator><creator>Zhang, Wanlu</creator><creator>Tang, Zhuqi</creator><creator>Wang, Cuifang</creator><creator>Zhu, Xiaohui</creator><creator>Cui, Shiwei</creator><general>Springer Netherlands</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></search><sort><creationdate>20151201</creationdate><title>KPNβ1 promotes palmitate-induced insulin resistance via NF-κB signaling in hepatocytes</title><author>Wang, Suxin ; Zhao, Yun ; Xia, Nana ; Zhang, Wanlu ; Tang, Zhuqi ; Wang, Cuifang ; Zhu, Xiaohui ; Cui, Shiwei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c329x-d88b46606d70472c5ec366b4609a9ed2e041a6339c7f4c327633f1cbca93a27e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Active Transport, Cell Nucleus</topic><topic>Animal Physiology</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Hep G2 Cells</topic><topic>Hepatocytes - metabolism</topic><topic>Human Physiology</topic><topic>Humans</topic><topic>Insulin - physiology</topic><topic>Insulin Resistance</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Male</topic><topic>Mice, Inbred C57BL</topic><topic>Nuclear Proteins - physiology</topic><topic>Original Paper</topic><topic>Palmitates</topic><topic>Signal Transduction</topic><topic>Transcription Factor RelA - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Suxin</creatorcontrib><creatorcontrib>Zhao, Yun</creatorcontrib><creatorcontrib>Xia, Nana</creatorcontrib><creatorcontrib>Zhang, Wanlu</creatorcontrib><creatorcontrib>Tang, Zhuqi</creatorcontrib><creatorcontrib>Wang, Cuifang</creatorcontrib><creatorcontrib>Zhu, Xiaohui</creatorcontrib><creatorcontrib>Cui, Shiwei</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><jtitle>Journal of physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Suxin</au><au>Zhao, Yun</au><au>Xia, Nana</au><au>Zhang, Wanlu</au><au>Tang, Zhuqi</au><au>Wang, Cuifang</au><au>Zhu, Xiaohui</au><au>Cui, Shiwei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>KPNβ1 promotes palmitate-induced insulin resistance via NF-κB signaling in hepatocytes</atitle><jtitle>Journal of physiology and biochemistry</jtitle><stitle>J Physiol Biochem</stitle><addtitle>J Physiol Biochem</addtitle><date>2015-12-01</date><risdate>2015</risdate><volume>71</volume><issue>4</issue><spage>763</spage><epage>772</epage><pages>763-772</pages><issn>1138-7548</issn><eissn>1877-8755</eissn><abstract>It has been intensively studied that inflammation contributes to the insulin resistance development in obesity-induced type 2 diabetes mellitus (T2DM). In this study, we assessed the effect of karyopherin β1 (KPNβ1) in hepatic insulin resistance and the underlying mechanisms using high-fat diet (HFD) fed mice and palmitate (PA)-stimulated hepatocytes (HepG2). KPNβ1 expression is increased in the HFD fed mice liver. PA upregulated KPNβ1 expression in HepG2 cells in a time-dependent manner. PA also increased pro-inflammatory cytokines expression, including tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and interleukin 1β (IL-1β). KPNβ1 knockdown reversed PA-induced pro-inflammatory cytokines expression and insulin-stimulated glucose uptake in HepG2 cells. In addition, KPNβ1 knockdown reduced intracellular lipid accumulation. Mechanistically, KPNβ1 transports nuclear factor kB (NF-κB) p65 from the cytoplasm to the nucleus to increase pro-inflammatory genes expression. In summary, KPNβ1 acts as a positive regulator in the NF-κB pathway to enhance palmitate-induced inflammation response and insulin resistance in HepG2 cells.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>26452501</pmid><doi>10.1007/s13105-015-0440-x</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1138-7548 |
| ispartof | Journal of physiology and biochemistry, 2015-12, Vol.71 (4), p.763-772 |
| issn | 1138-7548 1877-8755 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1744662810 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Active Transport, Cell Nucleus Animal Physiology Animals Biomedical and Life Sciences Biomedicine Hep G2 Cells Hepatocytes - metabolism Human Physiology Humans Insulin - physiology Insulin Resistance Liver - metabolism Liver - pathology Male Mice, Inbred C57BL Nuclear Proteins - physiology Original Paper Palmitates Signal Transduction Transcription Factor RelA - metabolism |
| title | KPNβ1 promotes palmitate-induced insulin resistance via NF-κB signaling in hepatocytes |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-06T03%3A26%3A46IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=KPN%CE%B21%20promotes%20palmitate-induced%20insulin%20resistance%20via%20NF-%CE%BAB%20signaling%20in%20hepatocytes&rft.jtitle=Journal%20of%20physiology%20and%20biochemistry&rft.au=Wang,%20Suxin&rft.date=2015-12-01&rft.volume=71&rft.issue=4&rft.spage=763&rft.epage=772&rft.pages=763-772&rft.issn=1138-7548&rft.eissn=1877-8755&rft_id=info:doi/10.1007/s13105-015-0440-x&rft_dat=%3Cproquest_cross%3E1744662810%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1744662810&rft_id=info:pmid/26452501&rfr_iscdi=true |