Angiotensin II-induced non-alcoholic fatty liver disease is mediated by oxidative stress in transgenic TG(mRen2)27(Ren2) rats
Background/Aims Non-alcoholic fatty liver disease (NAFLD) is a common health problem and includes a spectrum of hepatic steatosis, steatohepatitis and fibrosis. The renin–angiotensin system (RAS) plays a vital role in blood pressure regulation and appears to promote hepatic fibrogenesis. We hypothes...
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| Veröffentlicht in: | Journal of hepatology 2008-09, Vol.49 (3), p.417-428 |
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| creator | Wei, Yongzhong Clark, Suzanne E Morris, E. Matthew Thyfault, John P Uptergrove, Grace M.E Whaley-Connell, Adam T Ferrario, Carlos M Sowers, James R Ibdah, Jamal A |
| description | Background/Aims Non-alcoholic fatty liver disease (NAFLD) is a common health problem and includes a spectrum of hepatic steatosis, steatohepatitis and fibrosis. The renin–angiotensin system (RAS) plays a vital role in blood pressure regulation and appears to promote hepatic fibrogenesis. We hypothesized that increased RAS activity causes NAFLD due to increased hepatic oxidative stress. Methods We employed the transgenic TG(mRen2)27(Ren2) hypertensive rat, harboring the mouse renin gene with elevated tissue Angiotensin II (Ang II). Results Compared with normotensive Sprague–Dawley (SD) control rats, Ren2 developed significant hepatic steatosis by 9 weeks of age that progressed to marked steatohepatitis and fibrosis by 12 weeks. These changes were associated with increased levels of hepatic reactive oxygen species (ROS) and lipid peroxidation. Accordingly, 9-week-old Ren2 rats were treated for 3 weeks with valsartan, an angiotensin type 1 receptor blocker, or tempol, a superoxide dismutase/catalase mimetic. Hepatic indices for oxidative stress, steatosis, inflammation and fibrosis were markedly attenuated by both valsartan and tempol treatment. Conclusions This study suggests that Ang II causes development and progression of NAFLD in the transgenic Ren2 rat model by increasing hepatic ROS. Our findings also support a potential role of RAS in prevention and treatment of NAFLD. |
| doi_str_mv | 10.1016/j.jhep.2008.03.018 |
| format | Article |
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Matthew ; Thyfault, John P ; Uptergrove, Grace M.E ; Whaley-Connell, Adam T ; Ferrario, Carlos M ; Sowers, James R ; Ibdah, Jamal A</creator><creatorcontrib>Wei, Yongzhong ; Clark, Suzanne E ; Morris, E. Matthew ; Thyfault, John P ; Uptergrove, Grace M.E ; Whaley-Connell, Adam T ; Ferrario, Carlos M ; Sowers, James R ; Ibdah, Jamal A</creatorcontrib><description>Background/Aims Non-alcoholic fatty liver disease (NAFLD) is a common health problem and includes a spectrum of hepatic steatosis, steatohepatitis and fibrosis. The renin–angiotensin system (RAS) plays a vital role in blood pressure regulation and appears to promote hepatic fibrogenesis. We hypothesized that increased RAS activity causes NAFLD due to increased hepatic oxidative stress. Methods We employed the transgenic TG(mRen2)27(Ren2) hypertensive rat, harboring the mouse renin gene with elevated tissue Angiotensin II (Ang II). Results Compared with normotensive Sprague–Dawley (SD) control rats, Ren2 developed significant hepatic steatosis by 9 weeks of age that progressed to marked steatohepatitis and fibrosis by 12 weeks. These changes were associated with increased levels of hepatic reactive oxygen species (ROS) and lipid peroxidation. Accordingly, 9-week-old Ren2 rats were treated for 3 weeks with valsartan, an angiotensin type 1 receptor blocker, or tempol, a superoxide dismutase/catalase mimetic. Hepatic indices for oxidative stress, steatosis, inflammation and fibrosis were markedly attenuated by both valsartan and tempol treatment. Conclusions This study suggests that Ang II causes development and progression of NAFLD in the transgenic Ren2 rat model by increasing hepatic ROS. Our findings also support a potential role of RAS in prevention and treatment of NAFLD.</description><identifier>ISSN: 0168-8278</identifier><identifier>EISSN: 1600-0641</identifier><identifier>DOI: 10.1016/j.jhep.2008.03.018</identifier><identifier>PMID: 18486983</identifier><identifier>CODEN: JOHEEC</identifier><language>eng</language><publisher>Oxford: Elsevier B.V</publisher><subject>Angiotensin II ; Angiotensin II - physiology ; Animals ; Animals, Genetically Modified ; Antihypertensive Agents - pharmacology ; Antioxidants - pharmacology ; Apoptosis - drug effects ; Biological and medical sciences ; Blood Pressure - drug effects ; Blood Pressure - physiology ; Cyclic N-Oxides - pharmacology ; Disease Models, Animal ; Fatty Liver - metabolism ; Fatty Liver - physiopathology ; Gastroenterology and Hepatology ; Gastroenterology. Liver. Pancreas. Abdomen ; Lipid Peroxidation - drug effects ; Lipid Peroxidation - physiology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Non-alcoholic fatty liver disease ; Other diseases. Semiology ; Oxidative stress ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species - metabolism ; Renin - genetics ; Renin - metabolism ; Renin - physiology ; Renin-Angiotensin System - drug effects ; Renin-Angiotensin System - physiology ; Spin Labels ; Tetrazoles - pharmacology ; Valine - analogs & derivatives ; Valine - pharmacology ; Valsartan</subject><ispartof>Journal of hepatology, 2008-09, Vol.49 (3), p.417-428</ispartof><rights>European Association for the Study of the Liver</rights><rights>2008 European Association for the Study of the Liver</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c604t-8af39f941e6f6db4ddd525e9d03bcc2640199eb4a2c2287136f2649797c887af3</citedby><cites>FETCH-LOGICAL-c604t-8af39f941e6f6db4ddd525e9d03bcc2640199eb4a2c2287136f2649797c887af3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0168827808002316$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20627785$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18486983$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wei, Yongzhong</creatorcontrib><creatorcontrib>Clark, Suzanne E</creatorcontrib><creatorcontrib>Morris, E. Matthew</creatorcontrib><creatorcontrib>Thyfault, John P</creatorcontrib><creatorcontrib>Uptergrove, Grace M.E</creatorcontrib><creatorcontrib>Whaley-Connell, Adam T</creatorcontrib><creatorcontrib>Ferrario, Carlos M</creatorcontrib><creatorcontrib>Sowers, James R</creatorcontrib><creatorcontrib>Ibdah, Jamal A</creatorcontrib><title>Angiotensin II-induced non-alcoholic fatty liver disease is mediated by oxidative stress in transgenic TG(mRen2)27(Ren2) rats</title><title>Journal of hepatology</title><addtitle>J Hepatol</addtitle><description>Background/Aims Non-alcoholic fatty liver disease (NAFLD) is a common health problem and includes a spectrum of hepatic steatosis, steatohepatitis and fibrosis. The renin–angiotensin system (RAS) plays a vital role in blood pressure regulation and appears to promote hepatic fibrogenesis. We hypothesized that increased RAS activity causes NAFLD due to increased hepatic oxidative stress. Methods We employed the transgenic TG(mRen2)27(Ren2) hypertensive rat, harboring the mouse renin gene with elevated tissue Angiotensin II (Ang II). Results Compared with normotensive Sprague–Dawley (SD) control rats, Ren2 developed significant hepatic steatosis by 9 weeks of age that progressed to marked steatohepatitis and fibrosis by 12 weeks. These changes were associated with increased levels of hepatic reactive oxygen species (ROS) and lipid peroxidation. Accordingly, 9-week-old Ren2 rats were treated for 3 weeks with valsartan, an angiotensin type 1 receptor blocker, or tempol, a superoxide dismutase/catalase mimetic. Hepatic indices for oxidative stress, steatosis, inflammation and fibrosis were markedly attenuated by both valsartan and tempol treatment. Conclusions This study suggests that Ang II causes development and progression of NAFLD in the transgenic Ren2 rat model by increasing hepatic ROS. Our findings also support a potential role of RAS in prevention and treatment of NAFLD.</description><subject>Angiotensin II</subject><subject>Angiotensin II - physiology</subject><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Cyclic N-Oxides - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Fatty Liver - metabolism</subject><subject>Fatty Liver - physiopathology</subject><subject>Gastroenterology and Hepatology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Lipid Peroxidation - physiology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Non-alcoholic fatty liver disease</subject><subject>Other diseases. Semiology</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Renin - genetics</subject><subject>Renin - metabolism</subject><subject>Renin - physiology</subject><subject>Renin-Angiotensin System - drug effects</subject><subject>Renin-Angiotensin System - physiology</subject><subject>Spin Labels</subject><subject>Tetrazoles - pharmacology</subject><subject>Valine - analogs & derivatives</subject><subject>Valine - pharmacology</subject><subject>Valsartan</subject><issn>0168-8278</issn><issn>1600-0641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kl-LEzEUxQdR3Lr6BXyQvCjrw9SbZJrJgCwsi66FBUHX55Amd9rUaVKTtNgHv7sZW9Y_Dz4Fkt85Odxzq-o5hSkFKt6sp-sVbqcMQE6BT4HKB9WECoAaREMfVpMCyVqyVp5VT1JaAwCHrnlcnVHZSNFJPql-XPmlCxl9cp7M57XzdmfQEh98rQcTVmFwhvQ65wMZ3B4jsS6hTkhcIhu0TudCLw4kfHdW50KQlCOmRIpfjtqnJfricHdzsfmEnr1m7cWvk0Sd09PqUa-HhM9O53n15f27u-sP9e3Hm_n11W1tBDS5lrrnXd81FEUv7KKx1s7YDDsLfGEMEw3QrsNFo5lhTLaUi75cdm3XGinbIj6vLo--292ihDboS7RBbaPb6HhQQTv194t3K7UMe8WE5DMpisGrk0EM33aYstq4ZHAYtMewS0qUcLzlUEB2BE0MKUXs7z-hoMbW1FqNramxNQVcldaK6MWf8X5LTjUV4OUJ0MnooS9zNS7dcwwEa1s5K9zbI4dlmHuHUSXj0JdCXUSTlQ3u_zku_5GbwZX29PAVD5jWYRd9qUlRlZgC9Xncr3G9QAIwTgX_CSfszEM</recordid><startdate>20080901</startdate><enddate>20080901</enddate><creator>Wei, Yongzhong</creator><creator>Clark, Suzanne E</creator><creator>Morris, E. Matthew</creator><creator>Thyfault, John P</creator><creator>Uptergrove, Grace M.E</creator><creator>Whaley-Connell, Adam T</creator><creator>Ferrario, Carlos M</creator><creator>Sowers, James R</creator><creator>Ibdah, Jamal A</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><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>5PM</scope></search><sort><creationdate>20080901</creationdate><title>Angiotensin II-induced non-alcoholic fatty liver disease is mediated by oxidative stress in transgenic TG(mRen2)27(Ren2) rats</title><author>Wei, Yongzhong ; Clark, Suzanne E ; Morris, E. Matthew ; Thyfault, John P ; Uptergrove, Grace M.E ; Whaley-Connell, Adam T ; Ferrario, Carlos M ; Sowers, James R ; Ibdah, Jamal A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c604t-8af39f941e6f6db4ddd525e9d03bcc2640199eb4a2c2287136f2649797c887af3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Angiotensin II</topic><topic>Angiotensin II - physiology</topic><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>Antioxidants - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Pressure - physiology</topic><topic>Cyclic N-Oxides - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Fatty Liver - metabolism</topic><topic>Fatty Liver - physiopathology</topic><topic>Gastroenterology and Hepatology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Lipid Peroxidation - physiology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Non-alcoholic fatty liver disease</topic><topic>Other diseases. Semiology</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Renin - genetics</topic><topic>Renin - metabolism</topic><topic>Renin - physiology</topic><topic>Renin-Angiotensin System - drug effects</topic><topic>Renin-Angiotensin System - physiology</topic><topic>Spin Labels</topic><topic>Tetrazoles - pharmacology</topic><topic>Valine - analogs & derivatives</topic><topic>Valine - pharmacology</topic><topic>Valsartan</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wei, Yongzhong</creatorcontrib><creatorcontrib>Clark, Suzanne E</creatorcontrib><creatorcontrib>Morris, E. Matthew</creatorcontrib><creatorcontrib>Thyfault, John P</creatorcontrib><creatorcontrib>Uptergrove, Grace M.E</creatorcontrib><creatorcontrib>Whaley-Connell, Adam T</creatorcontrib><creatorcontrib>Ferrario, Carlos M</creatorcontrib><creatorcontrib>Sowers, James R</creatorcontrib><creatorcontrib>Ibdah, Jamal A</creatorcontrib><collection>Pascal-Francis</collection><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>PubMed Central (Full Participant titles)</collection><jtitle>Journal of hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wei, Yongzhong</au><au>Clark, Suzanne E</au><au>Morris, E. Matthew</au><au>Thyfault, John P</au><au>Uptergrove, Grace M.E</au><au>Whaley-Connell, Adam T</au><au>Ferrario, Carlos M</au><au>Sowers, James R</au><au>Ibdah, Jamal A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin II-induced non-alcoholic fatty liver disease is mediated by oxidative stress in transgenic TG(mRen2)27(Ren2) rats</atitle><jtitle>Journal of hepatology</jtitle><addtitle>J Hepatol</addtitle><date>2008-09-01</date><risdate>2008</risdate><volume>49</volume><issue>3</issue><spage>417</spage><epage>428</epage><pages>417-428</pages><issn>0168-8278</issn><eissn>1600-0641</eissn><coden>JOHEEC</coden><abstract>Background/Aims Non-alcoholic fatty liver disease (NAFLD) is a common health problem and includes a spectrum of hepatic steatosis, steatohepatitis and fibrosis. The renin–angiotensin system (RAS) plays a vital role in blood pressure regulation and appears to promote hepatic fibrogenesis. We hypothesized that increased RAS activity causes NAFLD due to increased hepatic oxidative stress. Methods We employed the transgenic TG(mRen2)27(Ren2) hypertensive rat, harboring the mouse renin gene with elevated tissue Angiotensin II (Ang II). Results Compared with normotensive Sprague–Dawley (SD) control rats, Ren2 developed significant hepatic steatosis by 9 weeks of age that progressed to marked steatohepatitis and fibrosis by 12 weeks. These changes were associated with increased levels of hepatic reactive oxygen species (ROS) and lipid peroxidation. Accordingly, 9-week-old Ren2 rats were treated for 3 weeks with valsartan, an angiotensin type 1 receptor blocker, or tempol, a superoxide dismutase/catalase mimetic. Hepatic indices for oxidative stress, steatosis, inflammation and fibrosis were markedly attenuated by both valsartan and tempol treatment. Conclusions This study suggests that Ang II causes development and progression of NAFLD in the transgenic Ren2 rat model by increasing hepatic ROS. Our findings also support a potential role of RAS in prevention and treatment of NAFLD.</abstract><cop>Oxford</cop><pub>Elsevier B.V</pub><pmid>18486983</pmid><doi>10.1016/j.jhep.2008.03.018</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiotensin II Angiotensin II - physiology Animals Animals, Genetically Modified Antihypertensive Agents - pharmacology Antioxidants - pharmacology Apoptosis - drug effects Biological and medical sciences Blood Pressure - drug effects Blood Pressure - physiology Cyclic N-Oxides - pharmacology Disease Models, Animal Fatty Liver - metabolism Fatty Liver - physiopathology Gastroenterology and Hepatology Gastroenterology. Liver. Pancreas. Abdomen Lipid Peroxidation - drug effects Lipid Peroxidation - physiology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Non-alcoholic fatty liver disease Other diseases. Semiology Oxidative stress Oxidative Stress - drug effects Oxidative Stress - physiology Rats Rats, Sprague-Dawley Reactive Oxygen Species - metabolism Renin - genetics Renin - metabolism Renin - physiology Renin-Angiotensin System - drug effects Renin-Angiotensin System - physiology Spin Labels Tetrazoles - pharmacology Valine - analogs & derivatives Valine - pharmacology Valsartan |
| title | Angiotensin II-induced non-alcoholic fatty liver disease is mediated by oxidative stress in transgenic TG(mRen2)27(Ren2) rats |
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