Targeted reduction of advanced glycation improves renal function in obesity
Obesity is highly prevalent in Western populations and is considered a risk factor for the development of renal impairment. Interventions that reduce the tissue burden of advanced glycation end-products (AGEs) have shown promise in stemming the progression of chronic disease. Here we tested if treat...
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| Veröffentlicht in: | Kidney international 2011-07, Vol.80 (2), p.190-198 |
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| creator | Harcourt, Brooke E. Sourris, Karly C. Coughlan, Melinda T. Walker, Karen Z. Dougherty, Sonia L. Andrikopoulos, Sofianos Morley, Amy L. Thallas-Bonke, Vicki Chand, Vibhasha Penfold, Sally A. de Courten, Maximilian P.J. Thomas, Merlin C. Kingwell, Bronwyn A. Bierhaus, Angelika Cooper, Mark E. Courten, Barbora de Forbes, Josephine M. |
| description | Obesity is highly prevalent in Western populations and is considered a risk factor for the development of renal impairment. Interventions that reduce the tissue burden of advanced glycation end-products (AGEs) have shown promise in stemming the progression of chronic disease. Here we tested if treatments that lower tissue AGE burden in patients and mice would improve obesity-related renal dysfunction. Overweight and obese individuals (body mass index (BMI) 26–39kg/m2) were recruited to a randomized, crossover clinical trial involving 2 weeks each on a low- and a high-AGE-containing diet. Renal function and an inflammatory profile (monocyte chemoattractant protein-1 (MCP-1) and macrophage migration inhibitory factor (MIF)) were improved following the low-AGE diet. Mechanisms of advanced glycation-related renal damage were investigated in a mouse model of obesity using the AGE-lowering pharmaceutical, alagebrium, and mice in which the receptor for AGE (RAGE) was deleted. Obesity, resulting from a diet high in both fat and AGE, caused renal impairment; however, treatment of the RAGE knockout mice with alagebrium improved urinary albumin excretion, creatinine clearance, the inflammatory profile, and renal oxidative stress. Alagebrium treatment, however, resulted in decreased weight gain and improved glycemic control compared with wild-type mice on a high-fat Western diet. Thus, targeted reduction of the advanced glycation pathway improved renal function in obesity. |
| doi_str_mv | 10.1038/ki.2011.57 |
| format | Article |
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Interventions that reduce the tissue burden of advanced glycation end-products (AGEs) have shown promise in stemming the progression of chronic disease. Here we tested if treatments that lower tissue AGE burden in patients and mice would improve obesity-related renal dysfunction. Overweight and obese individuals (body mass index (BMI) 26–39kg/m2) were recruited to a randomized, crossover clinical trial involving 2 weeks each on a low- and a high-AGE-containing diet. Renal function and an inflammatory profile (monocyte chemoattractant protein-1 (MCP-1) and macrophage migration inhibitory factor (MIF)) were improved following the low-AGE diet. Mechanisms of advanced glycation-related renal damage were investigated in a mouse model of obesity using the AGE-lowering pharmaceutical, alagebrium, and mice in which the receptor for AGE (RAGE) was deleted. Obesity, resulting from a diet high in both fat and AGE, caused renal impairment; however, treatment of the RAGE knockout mice with alagebrium improved urinary albumin excretion, creatinine clearance, the inflammatory profile, and renal oxidative stress. Alagebrium treatment, however, resulted in decreased weight gain and improved glycemic control compared with wild-type mice on a high-fat Western diet. Thus, targeted reduction of the advanced glycation pathway improved renal function in obesity.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/ki.2011.57</identifier><identifier>PMID: 21412218</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>Basingstoke: Elsevier Inc</publisher><subject>Adolescent ; Adult ; alagebrium chloride ; Animals ; Biological and medical sciences ; Cross-Over Studies ; Diet ; Glycation End Products, Advanced - administration & dosage ; Glycation End Products, Advanced - adverse effects ; Humans ; Inflammation - prevention & control ; Kidney - drug effects ; Kidney - physiopathology ; Kidney Diseases - chemically induced ; Kidney Diseases - diet therapy ; Kidney Diseases - drug therapy ; Male ; Medical sciences ; Metabolic diseases ; Mice ; Mice, Knockout ; Middle Aged ; Nephrology. Urinary tract diseases ; nephropathy ; Obesity ; Obesity - diet therapy ; Obesity - drug therapy ; Obesity - physiopathology ; RAGE ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic - deficiency ; Receptors, Immunologic - drug effects ; Thiazoles - pharmacology ; Thiazoles - therapeutic use ; Young Adult</subject><ispartof>Kidney international, 2011-07, Vol.80 (2), p.190-198</ispartof><rights>2011 International Society of Nephrology</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jul 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-1e6bbe0d2dc9b09c944000b7859e09bd0d7fd012bc217bd6e4dc1ed0df2b01fd3</citedby><cites>FETCH-LOGICAL-c490t-1e6bbe0d2dc9b09c944000b7859e09bd0d7fd012bc217bd6e4dc1ed0df2b01fd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24336353$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21412218$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Harcourt, Brooke E.</creatorcontrib><creatorcontrib>Sourris, Karly C.</creatorcontrib><creatorcontrib>Coughlan, Melinda T.</creatorcontrib><creatorcontrib>Walker, Karen Z.</creatorcontrib><creatorcontrib>Dougherty, Sonia L.</creatorcontrib><creatorcontrib>Andrikopoulos, Sofianos</creatorcontrib><creatorcontrib>Morley, Amy L.</creatorcontrib><creatorcontrib>Thallas-Bonke, Vicki</creatorcontrib><creatorcontrib>Chand, Vibhasha</creatorcontrib><creatorcontrib>Penfold, Sally A.</creatorcontrib><creatorcontrib>de Courten, Maximilian P.J.</creatorcontrib><creatorcontrib>Thomas, Merlin C.</creatorcontrib><creatorcontrib>Kingwell, Bronwyn A.</creatorcontrib><creatorcontrib>Bierhaus, Angelika</creatorcontrib><creatorcontrib>Cooper, Mark E.</creatorcontrib><creatorcontrib>Courten, Barbora de</creatorcontrib><creatorcontrib>Forbes, Josephine M.</creatorcontrib><title>Targeted reduction of advanced glycation improves renal function in obesity</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Obesity is highly prevalent in Western populations and is considered a risk factor for the development of renal impairment. Interventions that reduce the tissue burden of advanced glycation end-products (AGEs) have shown promise in stemming the progression of chronic disease. Here we tested if treatments that lower tissue AGE burden in patients and mice would improve obesity-related renal dysfunction. Overweight and obese individuals (body mass index (BMI) 26–39kg/m2) were recruited to a randomized, crossover clinical trial involving 2 weeks each on a low- and a high-AGE-containing diet. Renal function and an inflammatory profile (monocyte chemoattractant protein-1 (MCP-1) and macrophage migration inhibitory factor (MIF)) were improved following the low-AGE diet. Mechanisms of advanced glycation-related renal damage were investigated in a mouse model of obesity using the AGE-lowering pharmaceutical, alagebrium, and mice in which the receptor for AGE (RAGE) was deleted. Obesity, resulting from a diet high in both fat and AGE, caused renal impairment; however, treatment of the RAGE knockout mice with alagebrium improved urinary albumin excretion, creatinine clearance, the inflammatory profile, and renal oxidative stress. Alagebrium treatment, however, resulted in decreased weight gain and improved glycemic control compared with wild-type mice on a high-fat Western diet. Thus, targeted reduction of the advanced glycation pathway improved renal function in obesity.</description><subject>Adolescent</subject><subject>Adult</subject><subject>alagebrium chloride</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cross-Over Studies</subject><subject>Diet</subject><subject>Glycation End Products, Advanced - administration & dosage</subject><subject>Glycation End Products, Advanced - adverse effects</subject><subject>Humans</subject><subject>Inflammation - prevention & control</subject><subject>Kidney - drug effects</subject><subject>Kidney - physiopathology</subject><subject>Kidney Diseases - chemically induced</subject><subject>Kidney Diseases - diet therapy</subject><subject>Kidney Diseases - drug therapy</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Middle Aged</subject><subject>Nephrology. Urinary tract diseases</subject><subject>nephropathy</subject><subject>Obesity</subject><subject>Obesity - diet therapy</subject><subject>Obesity - drug therapy</subject><subject>Obesity - physiopathology</subject><subject>RAGE</subject><subject>Receptor for Advanced Glycation End Products</subject><subject>Receptors, Immunologic - deficiency</subject><subject>Receptors, Immunologic - drug effects</subject><subject>Thiazoles - pharmacology</subject><subject>Thiazoles - therapeutic use</subject><subject>Young Adult</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkFtLwzAYhoMobh5u_AEyBBGEzhzX9lKGJxx4M69DDl9Htq6dSTvYvze1U0G8CCEvT77v5UHoguAxwSy7W7kxxYSMRXqAhkRQlpBUiEM0xDgTCRUsG6CTEJY4vnOGj9GAEk4oJdkQvc6VX0ADduTBtqZxdTWqi5GyW1WZmC7KnVFfqVtvfL2FEMFKlaOirXraxQ8agmt2Z-ioUGWA8_19it4fH-bT52T29vQyvZ8lhue4SQhMtAZsqTW5xrnJOY_NdJqJHHCuLbZpYTGh2lCSajsBbg2BGBdUY1JYdopu-rmx0EcLoZFrFwyUpaqgboPMUs7jYWkkr_6Qy7r1sX6Eck5SljEWodseMr4OwUMhN96tld9JgmUnWK6c7ARL0U283E9s9RrsD_ptNALXe0AFo8rCR48u_HKcsQkT3VbecxBNbR14GYyDzrnzYBppa_ff_k_Uu5T4</recordid><startdate>20110701</startdate><enddate>20110701</enddate><creator>Harcourt, Brooke E.</creator><creator>Sourris, Karly C.</creator><creator>Coughlan, Melinda T.</creator><creator>Walker, Karen Z.</creator><creator>Dougherty, Sonia L.</creator><creator>Andrikopoulos, Sofianos</creator><creator>Morley, Amy L.</creator><creator>Thallas-Bonke, Vicki</creator><creator>Chand, Vibhasha</creator><creator>Penfold, Sally A.</creator><creator>de Courten, Maximilian P.J.</creator><creator>Thomas, Merlin C.</creator><creator>Kingwell, Bronwyn A.</creator><creator>Bierhaus, Angelika</creator><creator>Cooper, Mark E.</creator><creator>Courten, Barbora de</creator><creator>Forbes, Josephine M.</creator><general>Elsevier Inc</general><general>Nature Publishing Group</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><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>3V.</scope><scope>7QP</scope><scope>7RV</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>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20110701</creationdate><title>Targeted reduction of advanced glycation improves renal function in obesity</title><author>Harcourt, Brooke E. ; Sourris, Karly C. ; Coughlan, Melinda T. ; Walker, Karen Z. ; Dougherty, Sonia L. ; Andrikopoulos, Sofianos ; Morley, Amy L. ; Thallas-Bonke, Vicki ; Chand, Vibhasha ; Penfold, Sally A. ; de Courten, Maximilian P.J. ; Thomas, Merlin C. ; Kingwell, Bronwyn A. ; Bierhaus, Angelika ; Cooper, Mark E. ; Courten, Barbora de ; Forbes, Josephine M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-1e6bbe0d2dc9b09c944000b7859e09bd0d7fd012bc217bd6e4dc1ed0df2b01fd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>alagebrium chloride</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cross-Over Studies</topic><topic>Diet</topic><topic>Glycation End Products, Advanced - administration & dosage</topic><topic>Glycation End Products, Advanced - adverse effects</topic><topic>Humans</topic><topic>Inflammation - prevention & control</topic><topic>Kidney - drug effects</topic><topic>Kidney - physiopathology</topic><topic>Kidney Diseases - chemically induced</topic><topic>Kidney Diseases - diet therapy</topic><topic>Kidney Diseases - drug therapy</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Middle Aged</topic><topic>Nephrology. Urinary tract diseases</topic><topic>nephropathy</topic><topic>Obesity</topic><topic>Obesity - diet therapy</topic><topic>Obesity - drug therapy</topic><topic>Obesity - physiopathology</topic><topic>RAGE</topic><topic>Receptor for Advanced Glycation End Products</topic><topic>Receptors, Immunologic - deficiency</topic><topic>Receptors, Immunologic - drug effects</topic><topic>Thiazoles - pharmacology</topic><topic>Thiazoles - therapeutic use</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Harcourt, Brooke E.</creatorcontrib><creatorcontrib>Sourris, Karly C.</creatorcontrib><creatorcontrib>Coughlan, Melinda T.</creatorcontrib><creatorcontrib>Walker, Karen Z.</creatorcontrib><creatorcontrib>Dougherty, Sonia L.</creatorcontrib><creatorcontrib>Andrikopoulos, Sofianos</creatorcontrib><creatorcontrib>Morley, Amy L.</creatorcontrib><creatorcontrib>Thallas-Bonke, Vicki</creatorcontrib><creatorcontrib>Chand, Vibhasha</creatorcontrib><creatorcontrib>Penfold, Sally A.</creatorcontrib><creatorcontrib>de Courten, Maximilian P.J.</creatorcontrib><creatorcontrib>Thomas, Merlin C.</creatorcontrib><creatorcontrib>Kingwell, Bronwyn A.</creatorcontrib><creatorcontrib>Bierhaus, Angelika</creatorcontrib><creatorcontrib>Cooper, Mark E.</creatorcontrib><creatorcontrib>Courten, Barbora de</creatorcontrib><creatorcontrib>Forbes, Josephine M.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Proquest Nursing & Allied Health Source</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>Nursing & Allied Health Premium</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><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Harcourt, Brooke E.</au><au>Sourris, Karly C.</au><au>Coughlan, Melinda T.</au><au>Walker, Karen Z.</au><au>Dougherty, Sonia L.</au><au>Andrikopoulos, Sofianos</au><au>Morley, Amy L.</au><au>Thallas-Bonke, Vicki</au><au>Chand, Vibhasha</au><au>Penfold, Sally A.</au><au>de Courten, Maximilian P.J.</au><au>Thomas, Merlin C.</au><au>Kingwell, Bronwyn A.</au><au>Bierhaus, Angelika</au><au>Cooper, Mark E.</au><au>Courten, Barbora de</au><au>Forbes, Josephine M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeted reduction of advanced glycation improves renal function in obesity</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2011-07-01</date><risdate>2011</risdate><volume>80</volume><issue>2</issue><spage>190</spage><epage>198</epage><pages>190-198</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Obesity is highly prevalent in Western populations and is considered a risk factor for the development of renal impairment. Interventions that reduce the tissue burden of advanced glycation end-products (AGEs) have shown promise in stemming the progression of chronic disease. Here we tested if treatments that lower tissue AGE burden in patients and mice would improve obesity-related renal dysfunction. Overweight and obese individuals (body mass index (BMI) 26–39kg/m2) were recruited to a randomized, crossover clinical trial involving 2 weeks each on a low- and a high-AGE-containing diet. Renal function and an inflammatory profile (monocyte chemoattractant protein-1 (MCP-1) and macrophage migration inhibitory factor (MIF)) were improved following the low-AGE diet. Mechanisms of advanced glycation-related renal damage were investigated in a mouse model of obesity using the AGE-lowering pharmaceutical, alagebrium, and mice in which the receptor for AGE (RAGE) was deleted. Obesity, resulting from a diet high in both fat and AGE, caused renal impairment; however, treatment of the RAGE knockout mice with alagebrium improved urinary albumin excretion, creatinine clearance, the inflammatory profile, and renal oxidative stress. Alagebrium treatment, however, resulted in decreased weight gain and improved glycemic control compared with wild-type mice on a high-fat Western diet. Thus, targeted reduction of the advanced glycation pathway improved renal function in obesity.</abstract><cop>Basingstoke</cop><pub>Elsevier Inc</pub><pmid>21412218</pmid><doi>10.1038/ki.2011.57</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Kidney international, 2011-07, Vol.80 (2), p.190-198 |
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| subjects | Adolescent Adult alagebrium chloride Animals Biological and medical sciences Cross-Over Studies Diet Glycation End Products, Advanced - administration & dosage Glycation End Products, Advanced - adverse effects Humans Inflammation - prevention & control Kidney - drug effects Kidney - physiopathology Kidney Diseases - chemically induced Kidney Diseases - diet therapy Kidney Diseases - drug therapy Male Medical sciences Metabolic diseases Mice Mice, Knockout Middle Aged Nephrology. Urinary tract diseases nephropathy Obesity Obesity - diet therapy Obesity - drug therapy Obesity - physiopathology RAGE Receptor for Advanced Glycation End Products Receptors, Immunologic - deficiency Receptors, Immunologic - drug effects Thiazoles - pharmacology Thiazoles - therapeutic use Young Adult |
| title | Targeted reduction of advanced glycation improves renal function in obesity |
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