Aging Linked to Type 2 Diabetes Increases Oxidative Stress and Chronic Inflammation

Oxidative stress (OxS) and inflammation are physiopathological mechanisms related to diabetes and aging. We evaluated the additive effect of diabetes and aging on OxS and inflammation in a cross-sectional comparative study of 228 subjects: (1) 56 healthy adults (mean age, 47 ± 7 years); (2) 60 diabe...

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Veröffentlicht in:Rejuvenation research 2011-02, Vol.14 (1), p.25-31
Hauptverfasser: Mendoza-Núñez, Víctor Manuel, Rosado-Pérez, Juana, Santiago-Osorio, Edelmiro, Ortiz, Rocío, Sánchez-Rodríguez, Martha A., Galván-Duarte, Rosa Elba
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container_issue 1
container_start_page 25
container_title Rejuvenation research
container_volume 14
creator Mendoza-Núñez, Víctor Manuel
Rosado-Pérez, Juana
Santiago-Osorio, Edelmiro
Ortiz, Rocío
Sánchez-Rodríguez, Martha A.
Galván-Duarte, Rosa Elba
description Oxidative stress (OxS) and inflammation are physiopathological mechanisms related to diabetes and aging. We evaluated the additive effect of diabetes and aging on OxS and inflammation in a cross-sectional comparative study of 228 subjects: (1) 56 healthy adults (mean age, 47 ± 7 years); (2) 60 diabetic adults (mean age, 52 ± 6 years); (3) 40 healthy elderly adults (mean age, 67 ± 7 years); and (4) 72 diabetic elderly adults (mean age, 68 ± 7 years). We measured levels of glycosylated hemoglobin (HbA1c), plasma lipid peroxides, superoxide dismutase, glutathione peroxidase, total antioxidants, and tumor necrosis factor-alpha (TNF-α). The results indicate that diabetes is a risk factor for subjects with high serum levels of TNF-α (odds ratio [OR] = 12.1; 95% confidence interval [95% CI], 5.0–28; p  
doi_str_mv 10.1089/rej.2010.1054
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We evaluated the additive effect of diabetes and aging on OxS and inflammation in a cross-sectional comparative study of 228 subjects: (1) 56 healthy adults (mean age, 47 ± 7 years); (2) 60 diabetic adults (mean age, 52 ± 6 years); (3) 40 healthy elderly adults (mean age, 67 ± 7 years); and (4) 72 diabetic elderly adults (mean age, 68 ± 7 years). We measured levels of glycosylated hemoglobin (HbA1c), plasma lipid peroxides, superoxide dismutase, glutathione peroxidase, total antioxidants, and tumor necrosis factor-alpha (TNF-α). The results indicate that diabetes is a risk factor for subjects with high serum levels of TNF-α (odds ratio [OR] = 12.1; 95% confidence interval [95% CI], 5.0–28; p  &lt; 0.001); this correlation becomes stronger when it is also associated with aging (OR = 14; 95% CI, 3.7–53.7; p  &lt; 0.05). Likewise, we observed that diabetes is an independent risk factor for OxS (OR = 2.1; 95% CI, 1.2–3.8; p  &lt; 0.05), and a stronger factor in older patients (OR = 3.1; 95% CI, 1.3–7.5; p  &lt; 0.05). 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We evaluated the additive effect of diabetes and aging on OxS and inflammation in a cross-sectional comparative study of 228 subjects: (1) 56 healthy adults (mean age, 47 ± 7 years); (2) 60 diabetic adults (mean age, 52 ± 6 years); (3) 40 healthy elderly adults (mean age, 67 ± 7 years); and (4) 72 diabetic elderly adults (mean age, 68 ± 7 years). We measured levels of glycosylated hemoglobin (HbA1c), plasma lipid peroxides, superoxide dismutase, glutathione peroxidase, total antioxidants, and tumor necrosis factor-alpha (TNF-α). The results indicate that diabetes is a risk factor for subjects with high serum levels of TNF-α (odds ratio [OR] = 12.1; 95% confidence interval [95% CI], 5.0–28; p  &lt; 0.001); this correlation becomes stronger when it is also associated with aging (OR = 14; 95% CI, 3.7–53.7; p  &lt; 0.05). Likewise, we observed that diabetes is an independent risk factor for OxS (OR = 2.1; 95% CI, 1.2–3.8; p  &lt; 0.05), and a stronger factor in older patients (OR = 3.1; 95% CI, 1.3–7.5; p  &lt; 0.05). Our findings suggest that aging, in concert with diabetes, exerts an additive effect on OxS and inflammation.</description><subject>Aged</subject><subject>Aging</subject><subject>Aging - pathology</subject><subject>Biomarkers - blood</subject><subject>C-Reactive Protein - metabolism</subject><subject>Care and treatment</subject><subject>Case-Control Studies</subject><subject>Demographic aspects</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Diagnosis</subject><subject>Female</subject><subject>Humans</subject><subject>Hyperinsulinism - blood</subject><subject>Hyperinsulinism - complications</subject><subject>Hyperinsulinism - pathology</subject><subject>Inflammation</subject><subject>Inflammation - blood</subject><subject>Inflammation - complications</subject><subject>Inflammation - pathology</subject><subject>Influence</subject><subject>Interleukin-6 - blood</subject><subject>Male</subject><subject>Metabolic Syndrome - blood</subject><subject>Metabolic Syndrome - complications</subject><subject>Metabolic Syndrome - pathology</subject><subject>Middle Aged</subject><subject>Original Articles</subject><subject>Oxidative Stress</subject><subject>Physiological aspects</subject><subject>Risk Factors</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Type 2 diabetes</subject><issn>1549-1684</issn><issn>1557-8577</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtLAzEQgIMoPqpHrxLw4Glrkk262WOpTyh4aD2HbHa2pu5ma7IV--_N2ioIgswhk5lvhoEPoXNKhpTI_NrDcsjI10_wPXRMhcgSKbJsv895ntCR5EfoJIQlISzLhThER4wywkc8P0az8cK6BZ5a9wol7lo836wAM3xjdQEdBPzojAcdYvb0YUvd2XfAs85DCFi7Ek9efOusiVhV66aJ_dadooNK1wHOdu8APd_dzicPyfTp_nEyniaGk7RLgHGmGSHEECFLKFIKOeSSSmrKisUTtRYm54xzYgQTABUQSAvBeUHpiGbpAF1t9658-7aG0KnGBgN1rR2066CkYDllkpJIXm7Jha5BWVe1ndemp9WYCcIzmkoRqeEfVIwSGmtaB5WN9V8DyXbA-DYED5Vaedtov1GUqN6OinZUb0f1diJ_sTt4XTRQ_tDfOiKQboG-rJ2rLRTgu3_WfgIZEJj7</recordid><startdate>20110201</startdate><enddate>20110201</enddate><creator>Mendoza-Núñez, Víctor Manuel</creator><creator>Rosado-Pérez, Juana</creator><creator>Santiago-Osorio, Edelmiro</creator><creator>Ortiz, Rocío</creator><creator>Sánchez-Rodríguez, Martha A.</creator><creator>Galván-Duarte, Rosa Elba</creator><general>Mary Ann Liebert, 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>20110201</creationdate><title>Aging Linked to Type 2 Diabetes Increases Oxidative Stress and Chronic Inflammation</title><author>Mendoza-Núñez, Víctor Manuel ; Rosado-Pérez, Juana ; Santiago-Osorio, Edelmiro ; Ortiz, Rocío ; Sánchez-Rodríguez, Martha A. ; Galván-Duarte, Rosa Elba</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c403t-e242a2000c058deb31e9e98181cdf2212aa5c942440c525eefe0e3b544b116173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Aged</topic><topic>Aging</topic><topic>Aging - pathology</topic><topic>Biomarkers - blood</topic><topic>C-Reactive Protein - metabolism</topic><topic>Care and treatment</topic><topic>Case-Control Studies</topic><topic>Demographic aspects</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Diagnosis</topic><topic>Female</topic><topic>Humans</topic><topic>Hyperinsulinism - blood</topic><topic>Hyperinsulinism - complications</topic><topic>Hyperinsulinism - pathology</topic><topic>Inflammation</topic><topic>Inflammation - blood</topic><topic>Inflammation - complications</topic><topic>Inflammation - pathology</topic><topic>Influence</topic><topic>Interleukin-6 - blood</topic><topic>Male</topic><topic>Metabolic Syndrome - blood</topic><topic>Metabolic Syndrome - complications</topic><topic>Metabolic Syndrome - pathology</topic><topic>Middle Aged</topic><topic>Original Articles</topic><topic>Oxidative Stress</topic><topic>Physiological aspects</topic><topic>Risk Factors</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mendoza-Núñez, Víctor Manuel</creatorcontrib><creatorcontrib>Rosado-Pérez, Juana</creatorcontrib><creatorcontrib>Santiago-Osorio, Edelmiro</creatorcontrib><creatorcontrib>Ortiz, Rocío</creatorcontrib><creatorcontrib>Sánchez-Rodríguez, Martha A.</creatorcontrib><creatorcontrib>Galván-Duarte, Rosa Elba</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>Rejuvenation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mendoza-Núñez, Víctor Manuel</au><au>Rosado-Pérez, Juana</au><au>Santiago-Osorio, Edelmiro</au><au>Ortiz, Rocío</au><au>Sánchez-Rodríguez, Martha A.</au><au>Galván-Duarte, Rosa Elba</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aging Linked to Type 2 Diabetes Increases Oxidative Stress and Chronic Inflammation</atitle><jtitle>Rejuvenation research</jtitle><addtitle>Rejuvenation Res</addtitle><date>2011-02-01</date><risdate>2011</risdate><volume>14</volume><issue>1</issue><spage>25</spage><epage>31</epage><pages>25-31</pages><issn>1549-1684</issn><eissn>1557-8577</eissn><abstract>Oxidative stress (OxS) and inflammation are physiopathological mechanisms related to diabetes and aging. We evaluated the additive effect of diabetes and aging on OxS and inflammation in a cross-sectional comparative study of 228 subjects: (1) 56 healthy adults (mean age, 47 ± 7 years); (2) 60 diabetic adults (mean age, 52 ± 6 years); (3) 40 healthy elderly adults (mean age, 67 ± 7 years); and (4) 72 diabetic elderly adults (mean age, 68 ± 7 years). We measured levels of glycosylated hemoglobin (HbA1c), plasma lipid peroxides, superoxide dismutase, glutathione peroxidase, total antioxidants, and tumor necrosis factor-alpha (TNF-α). The results indicate that diabetes is a risk factor for subjects with high serum levels of TNF-α (odds ratio [OR] = 12.1; 95% confidence interval [95% CI], 5.0–28; p  &lt; 0.001); this correlation becomes stronger when it is also associated with aging (OR = 14; 95% CI, 3.7–53.7; p  &lt; 0.05). Likewise, we observed that diabetes is an independent risk factor for OxS (OR = 2.1; 95% CI, 1.2–3.8; p  &lt; 0.05), and a stronger factor in older patients (OR = 3.1; 95% CI, 1.3–7.5; p  &lt; 0.05). Our findings suggest that aging, in concert with diabetes, exerts an additive effect on OxS and inflammation.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>21204649</pmid><doi>10.1089/rej.2010.1054</doi><tpages>7</tpages></addata></record>
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subjects Aged
Aging
Aging - pathology
Biomarkers - blood
C-Reactive Protein - metabolism
Care and treatment
Case-Control Studies
Demographic aspects
Diabetes Mellitus, Type 2 - blood
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - pathology
Diagnosis
Female
Humans
Hyperinsulinism - blood
Hyperinsulinism - complications
Hyperinsulinism - pathology
Inflammation
Inflammation - blood
Inflammation - complications
Inflammation - pathology
Influence
Interleukin-6 - blood
Male
Metabolic Syndrome - blood
Metabolic Syndrome - complications
Metabolic Syndrome - pathology
Middle Aged
Original Articles
Oxidative Stress
Physiological aspects
Risk Factors
Tumor Necrosis Factor-alpha - blood
Type 2 diabetes
title Aging Linked to Type 2 Diabetes Increases Oxidative Stress and Chronic Inflammation
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