Increased expression of NAD(P)H oxidase in islets of animal models of Type 2 diabetes and its improvement by an AT1 receptor antagonist
This study was undertaken to reveal the role of NAD(P)H oxidase in increased oxidative stress in islets of Type 2 diabetes. Immunostaining analysis showed that staining intensities of NAD(P)H oxidase components, gp91phox and p22phox, significantly increased in islets of animal models of Type 2 diabe...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2005-07, Vol.332 (4), p.927-933 |
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| creator | Nakayama, Mieko Inoguchi, Toyoshi Sonta, Toshiyo Maeda, Yasutaka Sasaki, Shuji Sawada, Fumi Tsubouchi, Hirotaka Sonoda, Noriyuki Kobayashi, Kunihisa Sumimoto, Hideki Nawata, Hajime |
| description | This study was undertaken to reveal the role of NAD(P)H oxidase in increased oxidative stress in islets of Type 2 diabetes. Immunostaining analysis showed that staining intensities of NAD(P)H oxidase components, gp91phox and p22phox, significantly increased in islets of animal models of Type 2 diabetes, OLETF rats (60 weeks of age) and db/db mice (14 weeks of age), compared with age-matched controls, respectively, correlating with increased levels of oxidative stress marker, 8-hydroxy-deoxyguanosine or 4-hydroxy-2-nonenal modified protein. In db/db mice, oral administration of angiotensin II Type 1 receptor antagonist valsartan (5
mg/kg) for 4 weeks significantly attenuated the increased expression of gp91phox and p22phox together with inhibition of oxidative stress and partially restored decreased insulin contents in islets. Angiotensin II-related increased expression of NAD(P)H oxidase may play an important role in increased oxidative stress in islets of Type 2 diabetes. This mechanism may be a novel therapeutic target for preventing β-cell damage. |
| doi_str_mv | 10.1016/j.bbrc.2005.05.065 |
| format | Article |
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mg/kg) for 4 weeks significantly attenuated the increased expression of gp91phox and p22phox together with inhibition of oxidative stress and partially restored decreased insulin contents in islets. Angiotensin II-related increased expression of NAD(P)H oxidase may play an important role in increased oxidative stress in islets of Type 2 diabetes. This mechanism may be a novel therapeutic target for preventing β-cell damage.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2005.05.065</identifier><identifier>PMID: 15922295</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Administration, Oral ; Aldehydes - pharmacology ; Angiotensin II ; Angiotensin II - metabolism ; Angiotensin II Type 1 Receptor Blockers - pharmacology ; Angiotensins - metabolism ; Animals ; Body Weight ; Deoxyguanosine - analogs & derivatives ; Deoxyguanosine - pharmacology ; Diabetes Mellitus, Type 2 - metabolism ; Disease Models, Animal ; Insulin - metabolism ; Islets of Langerhans - enzymology ; Islets of Langerhans - metabolism ; Membrane Glycoproteins - metabolism ; Membrane Transport Proteins - metabolism ; Mice ; Mice, Inbred C57BL ; NAD(P)H oxidase ; NADPH Oxidase 2 ; NADPH Oxidases - biosynthesis ; NADPH Oxidases - metabolism ; Oxidative Stress ; Phosphoproteins - metabolism ; Rats ; Rats, Inbred OLETF ; Rats, Long-Evans ; Tetrazoles - pharmacology ; Time Factors ; Type 2 diabetes ; Valine - analogs & derivatives ; Valine - pharmacology ; Valsartan ; β-cell</subject><ispartof>Biochemical and biophysical research communications, 2005-07, Vol.332 (4), p.927-933</ispartof><rights>2005 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-885c4aac4c285b3d8c6856edbbc276fd743c5eff1abc2950198257ecaf0b07d53</citedby><cites>FETCH-LOGICAL-c420t-885c4aac4c285b3d8c6856edbbc276fd743c5eff1abc2950198257ecaf0b07d53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2005.05.065$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15922295$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nakayama, Mieko</creatorcontrib><creatorcontrib>Inoguchi, Toyoshi</creatorcontrib><creatorcontrib>Sonta, Toshiyo</creatorcontrib><creatorcontrib>Maeda, Yasutaka</creatorcontrib><creatorcontrib>Sasaki, Shuji</creatorcontrib><creatorcontrib>Sawada, Fumi</creatorcontrib><creatorcontrib>Tsubouchi, Hirotaka</creatorcontrib><creatorcontrib>Sonoda, Noriyuki</creatorcontrib><creatorcontrib>Kobayashi, Kunihisa</creatorcontrib><creatorcontrib>Sumimoto, Hideki</creatorcontrib><creatorcontrib>Nawata, Hajime</creatorcontrib><title>Increased expression of NAD(P)H oxidase in islets of animal models of Type 2 diabetes and its improvement by an AT1 receptor antagonist</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>This study was undertaken to reveal the role of NAD(P)H oxidase in increased oxidative stress in islets of Type 2 diabetes. Immunostaining analysis showed that staining intensities of NAD(P)H oxidase components, gp91phox and p22phox, significantly increased in islets of animal models of Type 2 diabetes, OLETF rats (60 weeks of age) and db/db mice (14 weeks of age), compared with age-matched controls, respectively, correlating with increased levels of oxidative stress marker, 8-hydroxy-deoxyguanosine or 4-hydroxy-2-nonenal modified protein. In db/db mice, oral administration of angiotensin II Type 1 receptor antagonist valsartan (5
mg/kg) for 4 weeks significantly attenuated the increased expression of gp91phox and p22phox together with inhibition of oxidative stress and partially restored decreased insulin contents in islets. Angiotensin II-related increased expression of NAD(P)H oxidase may play an important role in increased oxidative stress in islets of Type 2 diabetes. This mechanism may be a novel therapeutic target for preventing β-cell damage.</description><subject>Administration, Oral</subject><subject>Aldehydes - pharmacology</subject><subject>Angiotensin II</subject><subject>Angiotensin II - metabolism</subject><subject>Angiotensin II Type 1 Receptor Blockers - pharmacology</subject><subject>Angiotensins - metabolism</subject><subject>Animals</subject><subject>Body Weight</subject><subject>Deoxyguanosine - analogs & derivatives</subject><subject>Deoxyguanosine - pharmacology</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Disease Models, Animal</subject><subject>Insulin - metabolism</subject><subject>Islets of Langerhans - enzymology</subject><subject>Islets of Langerhans - metabolism</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Membrane Transport Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NAD(P)H oxidase</subject><subject>NADPH Oxidase 2</subject><subject>NADPH Oxidases - biosynthesis</subject><subject>NADPH Oxidases - metabolism</subject><subject>Oxidative Stress</subject><subject>Phosphoproteins - metabolism</subject><subject>Rats</subject><subject>Rats, Inbred OLETF</subject><subject>Rats, Long-Evans</subject><subject>Tetrazoles - pharmacology</subject><subject>Time Factors</subject><subject>Type 2 diabetes</subject><subject>Valine - analogs & derivatives</subject><subject>Valine - pharmacology</subject><subject>Valsartan</subject><subject>β-cell</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM-KFDEQh4Mo7uzqC3iQnEQPPVYynXQ3eBlW111Y1MMI3kL-VEuG7k6bZJadJ_C1TTsD3oSCkKovPyofIa8YrBkw-X6_NibaNQcQ66WkeEJWDDqoOIP6KVkBgKx4x35ckMuU9gCM1bJ7Ti6Y6DjnnViR33eTjagTOoqPc8SUfJho6OmX7ce3397d0vDoXRlTP1GfBsxpGerJj3qgY3A4_G3sjjNSTp3XBjOmAjjqC-vHOYYHHHHK1BxLm253jEa0OOcQyz3rn2HyKb8gz3o9JHx5Pq_I95tPu-vb6v7r57vr7X1law65altha61tbXkrzMa1VrZCojPG8kb2rqk3VmDfM10anQDWtVw0aHUPBhonNlfkzSm37PXrgCmr0SeLw6AnDIekZNNx2AAvID-BNoaUIvZqjuXT8agYqEW_2qtFv1r0q6Xkkv76nH4wI7p_T86-C_DhBBRv-OAxqmQ9ThadL1KycsH_L_8P5iKXhQ</recordid><startdate>20050715</startdate><enddate>20050715</enddate><creator>Nakayama, Mieko</creator><creator>Inoguchi, Toyoshi</creator><creator>Sonta, Toshiyo</creator><creator>Maeda, Yasutaka</creator><creator>Sasaki, Shuji</creator><creator>Sawada, Fumi</creator><creator>Tsubouchi, Hirotaka</creator><creator>Sonoda, Noriyuki</creator><creator>Kobayashi, Kunihisa</creator><creator>Sumimoto, Hideki</creator><creator>Nawata, Hajime</creator><general>Elsevier Inc</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>20050715</creationdate><title>Increased expression of NAD(P)H oxidase in islets of animal models of Type 2 diabetes and its improvement by an AT1 receptor antagonist</title><author>Nakayama, Mieko ; Inoguchi, Toyoshi ; Sonta, Toshiyo ; Maeda, Yasutaka ; Sasaki, Shuji ; Sawada, Fumi ; Tsubouchi, Hirotaka ; Sonoda, Noriyuki ; Kobayashi, Kunihisa ; Sumimoto, Hideki ; Nawata, Hajime</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-885c4aac4c285b3d8c6856edbbc276fd743c5eff1abc2950198257ecaf0b07d53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Administration, Oral</topic><topic>Aldehydes - pharmacology</topic><topic>Angiotensin II</topic><topic>Angiotensin II - metabolism</topic><topic>Angiotensin II Type 1 Receptor Blockers - pharmacology</topic><topic>Angiotensins - metabolism</topic><topic>Animals</topic><topic>Body Weight</topic><topic>Deoxyguanosine - analogs & derivatives</topic><topic>Deoxyguanosine - pharmacology</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Disease Models, Animal</topic><topic>Insulin - metabolism</topic><topic>Islets of Langerhans - enzymology</topic><topic>Islets of Langerhans - metabolism</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Membrane Transport Proteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NAD(P)H oxidase</topic><topic>NADPH Oxidase 2</topic><topic>NADPH Oxidases - biosynthesis</topic><topic>NADPH Oxidases - metabolism</topic><topic>Oxidative Stress</topic><topic>Phosphoproteins - metabolism</topic><topic>Rats</topic><topic>Rats, Inbred OLETF</topic><topic>Rats, Long-Evans</topic><topic>Tetrazoles - pharmacology</topic><topic>Time Factors</topic><topic>Type 2 diabetes</topic><topic>Valine - analogs & derivatives</topic><topic>Valine - pharmacology</topic><topic>Valsartan</topic><topic>β-cell</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nakayama, Mieko</creatorcontrib><creatorcontrib>Inoguchi, Toyoshi</creatorcontrib><creatorcontrib>Sonta, Toshiyo</creatorcontrib><creatorcontrib>Maeda, Yasutaka</creatorcontrib><creatorcontrib>Sasaki, Shuji</creatorcontrib><creatorcontrib>Sawada, Fumi</creatorcontrib><creatorcontrib>Tsubouchi, Hirotaka</creatorcontrib><creatorcontrib>Sonoda, Noriyuki</creatorcontrib><creatorcontrib>Kobayashi, Kunihisa</creatorcontrib><creatorcontrib>Sumimoto, Hideki</creatorcontrib><creatorcontrib>Nawata, Hajime</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>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nakayama, Mieko</au><au>Inoguchi, Toyoshi</au><au>Sonta, Toshiyo</au><au>Maeda, Yasutaka</au><au>Sasaki, Shuji</au><au>Sawada, Fumi</au><au>Tsubouchi, Hirotaka</au><au>Sonoda, Noriyuki</au><au>Kobayashi, Kunihisa</au><au>Sumimoto, Hideki</au><au>Nawata, Hajime</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased expression of NAD(P)H oxidase in islets of animal models of Type 2 diabetes and its improvement by an AT1 receptor antagonist</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2005-07-15</date><risdate>2005</risdate><volume>332</volume><issue>4</issue><spage>927</spage><epage>933</epage><pages>927-933</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>This study was undertaken to reveal the role of NAD(P)H oxidase in increased oxidative stress in islets of Type 2 diabetes. Immunostaining analysis showed that staining intensities of NAD(P)H oxidase components, gp91phox and p22phox, significantly increased in islets of animal models of Type 2 diabetes, OLETF rats (60 weeks of age) and db/db mice (14 weeks of age), compared with age-matched controls, respectively, correlating with increased levels of oxidative stress marker, 8-hydroxy-deoxyguanosine or 4-hydroxy-2-nonenal modified protein. In db/db mice, oral administration of angiotensin II Type 1 receptor antagonist valsartan (5
mg/kg) for 4 weeks significantly attenuated the increased expression of gp91phox and p22phox together with inhibition of oxidative stress and partially restored decreased insulin contents in islets. Angiotensin II-related increased expression of NAD(P)H oxidase may play an important role in increased oxidative stress in islets of Type 2 diabetes. This mechanism may be a novel therapeutic target for preventing β-cell damage.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15922295</pmid><doi>10.1016/j.bbrc.2005.05.065</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Biochemical and biophysical research communications, 2005-07, Vol.332 (4), p.927-933 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Administration, Oral Aldehydes - pharmacology Angiotensin II Angiotensin II - metabolism Angiotensin II Type 1 Receptor Blockers - pharmacology Angiotensins - metabolism Animals Body Weight Deoxyguanosine - analogs & derivatives Deoxyguanosine - pharmacology Diabetes Mellitus, Type 2 - metabolism Disease Models, Animal Insulin - metabolism Islets of Langerhans - enzymology Islets of Langerhans - metabolism Membrane Glycoproteins - metabolism Membrane Transport Proteins - metabolism Mice Mice, Inbred C57BL NAD(P)H oxidase NADPH Oxidase 2 NADPH Oxidases - biosynthesis NADPH Oxidases - metabolism Oxidative Stress Phosphoproteins - metabolism Rats Rats, Inbred OLETF Rats, Long-Evans Tetrazoles - pharmacology Time Factors Type 2 diabetes Valine - analogs & derivatives Valine - pharmacology Valsartan β-cell |
| title | Increased expression of NAD(P)H oxidase in islets of animal models of Type 2 diabetes and its improvement by an AT1 receptor antagonist |
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