Urinary Excretion of Neutrophil Gelatinase-Associated Lipocalin in Diabetic Rats
Recent studies suggest that tubular damage precedes glomerular damage in the progression of diabetic nephropathy. Therefore, we evaluated oxidative stress and urinary excretion of tubular proteins as markers of tubular dysfunction. Methods. Diabetes was induced in rats by streptozotocin administrati...
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| creator | Osorio, Horacio Tapia, Edilia Loredo-Mendoza, María Lilia Cristóbal-García, Magdalena García-Arroyo, Fernando Enrique Arellano, Abraham Sánchez-Lozada, Laura Gabriela |
| description | Recent studies suggest that tubular damage precedes glomerular damage in the progression of diabetic nephropathy. Therefore, we evaluated oxidative stress and urinary excretion of tubular proteins as markers of tubular dysfunction. Methods. Diabetes was induced in rats by streptozotocin administration (50 mg/kg). Oxidative stress was assessed by measuring the activity of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD); additionally, expression levels of 3-nitrotyrosine (3-NT), 4-hydroxynonenal (4-HNE), and oxidized protein (OP) were quantified. Whole glomerular filtration rate (GFR) was measured. Urinary excretion of neutrophil gelatinase-associated lipocalin (uNGAL), osteopontin (uOPN), and N-acetyl-β-D-glucosaminidase (uNAG) was also determined. Results. Diabetic rats showed an increase in uNGAL excretion 7 days following induction of diabetes. Diuresis, proteinuria, albuminuria, creatinine clearance, and GFR were significantly increased by 30 days after induction. Furthermore, there was an increase in both CAT and SOD activity, in addition to 3-NT, 4-HNE, and OP expression levels. However, GPx activity was lower. Serum levels of NGAL and OPN, as well as excretion levels of uNGAL, uOPN, and uNAG, were increased in diabetics. Tubular damage was observed by 7 days after diabetes induction and was further aggravated by 30 days after induction. Conclusion. The tubular dysfunction evidenced by urinary excretion of NGAL precedes oxidative stress during diabetes. |
| doi_str_mv | 10.1155/2014/961326 |
| format | Article |
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Therefore, we evaluated oxidative stress and urinary excretion of tubular proteins as markers of tubular dysfunction. Methods. Diabetes was induced in rats by streptozotocin administration (50 mg/kg). Oxidative stress was assessed by measuring the activity of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD); additionally, expression levels of 3-nitrotyrosine (3-NT), 4-hydroxynonenal (4-HNE), and oxidized protein (OP) were quantified. Whole glomerular filtration rate (GFR) was measured. Urinary excretion of neutrophil gelatinase-associated lipocalin (uNGAL), osteopontin (uOPN), and N-acetyl-β-D-glucosaminidase (uNAG) was also determined. Results. Diabetic rats showed an increase in uNGAL excretion 7 days following induction of diabetes. Diuresis, proteinuria, albuminuria, creatinine clearance, and GFR were significantly increased by 30 days after induction. Furthermore, there was an increase in both CAT and SOD activity, in addition to 3-NT, 4-HNE, and OP expression levels. However, GPx activity was lower. Serum levels of NGAL and OPN, as well as excretion levels of uNGAL, uOPN, and uNAG, were increased in diabetics. Tubular damage was observed by 7 days after diabetes induction and was further aggravated by 30 days after induction. Conclusion. The tubular dysfunction evidenced by urinary excretion of NGAL precedes oxidative stress during diabetes.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2014/961326</identifier><identifier>PMID: 25243053</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Acute-Phase Proteins - urine ; Animals ; Biomarkers ; Biomarkers - urine ; Cardiovascular disease ; Carrier proteins ; Development and progression ; Diabetes ; Diabetes Mellitus, Experimental - pathology ; Diabetes Mellitus, Experimental - urine ; Diabetic nephropathies ; Diabetic Nephropathies - pathology ; Diabetic Nephropathies - urine ; Federal regulation ; Health aspects ; Heart surgery ; Hyperglycemia ; Laboratories ; Lipocalins - urine ; Male ; Metabolism ; Neutrophils ; Oxidative stress ; Oxidative Stress - physiology ; Proteins ; Proto-Oncogene Proteins - urine ; Rats ; Rats, Wistar ; Reactive Oxygen Species - metabolism ; Rodents ; Studies ; Urine</subject><ispartof>Oxidative medicine and cellular longevity, 2014-01, Vol.2014 (2014), p.1-11</ispartof><rights>Copyright © 2014 Abraham Said Arellano-Buendía et al.</rights><rights>COPYRIGHT 2014 John Wiley & Sons, Inc.</rights><rights>Copyright © 2014 Abraham Said Arellano-Buendia et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2014 Abraham Said Arellano-Buendía et al. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c495t-703a8e54868941d8f7dc8fccce3f4c540ac8954b0671e7119cd80ff62b17dc753</citedby><cites>FETCH-LOGICAL-c495t-703a8e54868941d8f7dc8fccce3f4c540ac8954b0671e7119cd80ff62b17dc753</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163304/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163304/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25243053$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Morishita, Ryuichi</contributor><creatorcontrib>Osorio, Horacio</creatorcontrib><creatorcontrib>Tapia, Edilia</creatorcontrib><creatorcontrib>Loredo-Mendoza, María Lilia</creatorcontrib><creatorcontrib>Cristóbal-García, Magdalena</creatorcontrib><creatorcontrib>García-Arroyo, Fernando Enrique</creatorcontrib><creatorcontrib>Arellano, Abraham</creatorcontrib><creatorcontrib>Sánchez-Lozada, Laura Gabriela</creatorcontrib><title>Urinary Excretion of Neutrophil Gelatinase-Associated Lipocalin in Diabetic Rats</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Recent studies suggest that tubular damage precedes glomerular damage in the progression of diabetic nephropathy. Therefore, we evaluated oxidative stress and urinary excretion of tubular proteins as markers of tubular dysfunction. Methods. Diabetes was induced in rats by streptozotocin administration (50 mg/kg). Oxidative stress was assessed by measuring the activity of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD); additionally, expression levels of 3-nitrotyrosine (3-NT), 4-hydroxynonenal (4-HNE), and oxidized protein (OP) were quantified. Whole glomerular filtration rate (GFR) was measured. Urinary excretion of neutrophil gelatinase-associated lipocalin (uNGAL), osteopontin (uOPN), and N-acetyl-β-D-glucosaminidase (uNAG) was also determined. Results. Diabetic rats showed an increase in uNGAL excretion 7 days following induction of diabetes. Diuresis, proteinuria, albuminuria, creatinine clearance, and GFR were significantly increased by 30 days after induction. Furthermore, there was an increase in both CAT and SOD activity, in addition to 3-NT, 4-HNE, and OP expression levels. However, GPx activity was lower. Serum levels of NGAL and OPN, as well as excretion levels of uNGAL, uOPN, and uNAG, were increased in diabetics. Tubular damage was observed by 7 days after diabetes induction and was further aggravated by 30 days after induction. Conclusion. The tubular dysfunction evidenced by urinary excretion of NGAL precedes oxidative stress during diabetes.</description><subject>Acute-Phase Proteins - urine</subject><subject>Animals</subject><subject>Biomarkers</subject><subject>Biomarkers - urine</subject><subject>Cardiovascular disease</subject><subject>Carrier proteins</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>Diabetes Mellitus, Experimental - urine</subject><subject>Diabetic nephropathies</subject><subject>Diabetic Nephropathies - pathology</subject><subject>Diabetic Nephropathies - urine</subject><subject>Federal regulation</subject><subject>Health aspects</subject><subject>Heart surgery</subject><subject>Hyperglycemia</subject><subject>Laboratories</subject><subject>Lipocalins - urine</subject><subject>Male</subject><subject>Metabolism</subject><subject>Neutrophils</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - physiology</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins - urine</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Rodents</subject><subject>Studies</subject><subject>Urine</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqN0c1rFDEYBvBBFFurJ-8y4EWUsXkn3xdhqbUKi4rYc8hm3nRTZpNtMuPHf2-WrWv1JAxkIL88ycvTNE-BvAbg_LQnwE61ANqLe80xaNZ3RGt2__BPyFHzqJRrQgTtGTxsjnreM0o4PW4-X-YQbf7Znv9wGaeQYpt8-xHnKaftOoztBY52qqRgtygluWAnHNpl2CZnxxDb-r0NdlWPuvaLncrj5oG3Y8Ent-tJc_nu_OvZ-2756eLD2WLZOab51ElCrULOlFCawaC8HJzyzjmknjnOiHVKc7YiQgJKAO0GRbwX_QqqlJyeNG_2udt5tcHBYZyyHc02h00dxyQbzN87MazNVfpmGAhKCasBL24DcrqZsUxmE4rDcbQR01wMcMEoZ1RBpc__oddpzrGOZ0ASzYQmIP-oKzuiCdGneq_bhZoFAwmES1BVvdorl1MpGf3hyUDMrk-z69Ps-6z62d0pD_Z3gRW83IN1iIP9Hv4vDStBb-9gJusk9Bf-_7Ao</recordid><startdate>20140101</startdate><enddate>20140101</enddate><creator>Osorio, Horacio</creator><creator>Tapia, Edilia</creator><creator>Loredo-Mendoza, María Lilia</creator><creator>Cristóbal-García, Magdalena</creator><creator>García-Arroyo, Fernando Enrique</creator><creator>Arellano, Abraham</creator><creator>Sánchez-Lozada, Laura Gabriela</creator><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140101</creationdate><title>Urinary Excretion of Neutrophil Gelatinase-Associated Lipocalin in Diabetic Rats</title><author>Osorio, Horacio ; Tapia, Edilia ; Loredo-Mendoza, María Lilia ; Cristóbal-García, Magdalena ; García-Arroyo, Fernando Enrique ; Arellano, Abraham ; Sánchez-Lozada, Laura Gabriela</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c495t-703a8e54868941d8f7dc8fccce3f4c540ac8954b0671e7119cd80ff62b17dc753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Acute-Phase Proteins - urine</topic><topic>Animals</topic><topic>Biomarkers</topic><topic>Biomarkers - urine</topic><topic>Cardiovascular disease</topic><topic>Carrier proteins</topic><topic>Development and progression</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Experimental - pathology</topic><topic>Diabetes Mellitus, Experimental - urine</topic><topic>Diabetic nephropathies</topic><topic>Diabetic Nephropathies - pathology</topic><topic>Diabetic Nephropathies - urine</topic><topic>Federal regulation</topic><topic>Health aspects</topic><topic>Heart surgery</topic><topic>Hyperglycemia</topic><topic>Laboratories</topic><topic>Lipocalins - urine</topic><topic>Male</topic><topic>Metabolism</topic><topic>Neutrophils</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - physiology</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins - urine</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Rodents</topic><topic>Studies</topic><topic>Urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Osorio, Horacio</creatorcontrib><creatorcontrib>Tapia, Edilia</creatorcontrib><creatorcontrib>Loredo-Mendoza, María Lilia</creatorcontrib><creatorcontrib>Cristóbal-García, Magdalena</creatorcontrib><creatorcontrib>García-Arroyo, Fernando Enrique</creatorcontrib><creatorcontrib>Arellano, Abraham</creatorcontrib><creatorcontrib>Sánchez-Lozada, Laura Gabriela</creatorcontrib><collection>الدوريات العلمية والإحصائية - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Osorio, Horacio</au><au>Tapia, Edilia</au><au>Loredo-Mendoza, María Lilia</au><au>Cristóbal-García, Magdalena</au><au>García-Arroyo, Fernando Enrique</au><au>Arellano, Abraham</au><au>Sánchez-Lozada, Laura Gabriela</au><au>Morishita, Ryuichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Urinary Excretion of Neutrophil Gelatinase-Associated Lipocalin in Diabetic Rats</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2014-01-01</date><risdate>2014</risdate><volume>2014</volume><issue>2014</issue><spage>1</spage><epage>11</epage><pages>1-11</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Recent studies suggest that tubular damage precedes glomerular damage in the progression of diabetic nephropathy. Therefore, we evaluated oxidative stress and urinary excretion of tubular proteins as markers of tubular dysfunction. Methods. Diabetes was induced in rats by streptozotocin administration (50 mg/kg). Oxidative stress was assessed by measuring the activity of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD); additionally, expression levels of 3-nitrotyrosine (3-NT), 4-hydroxynonenal (4-HNE), and oxidized protein (OP) were quantified. Whole glomerular filtration rate (GFR) was measured. Urinary excretion of neutrophil gelatinase-associated lipocalin (uNGAL), osteopontin (uOPN), and N-acetyl-β-D-glucosaminidase (uNAG) was also determined. Results. Diabetic rats showed an increase in uNGAL excretion 7 days following induction of diabetes. Diuresis, proteinuria, albuminuria, creatinine clearance, and GFR were significantly increased by 30 days after induction. Furthermore, there was an increase in both CAT and SOD activity, in addition to 3-NT, 4-HNE, and OP expression levels. However, GPx activity was lower. Serum levels of NGAL and OPN, as well as excretion levels of uNGAL, uOPN, and uNAG, were increased in diabetics. Tubular damage was observed by 7 days after diabetes induction and was further aggravated by 30 days after induction. Conclusion. The tubular dysfunction evidenced by urinary excretion of NGAL precedes oxidative stress during diabetes.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>25243053</pmid><doi>10.1155/2014/961326</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute-Phase Proteins - urine Animals Biomarkers Biomarkers - urine Cardiovascular disease Carrier proteins Development and progression Diabetes Diabetes Mellitus, Experimental - pathology Diabetes Mellitus, Experimental - urine Diabetic nephropathies Diabetic Nephropathies - pathology Diabetic Nephropathies - urine Federal regulation Health aspects Heart surgery Hyperglycemia Laboratories Lipocalins - urine Male Metabolism Neutrophils Oxidative stress Oxidative Stress - physiology Proteins Proto-Oncogene Proteins - urine Rats Rats, Wistar Reactive Oxygen Species - metabolism Rodents Studies Urine |
| title | Urinary Excretion of Neutrophil Gelatinase-Associated Lipocalin in Diabetic Rats |
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