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Association between fasting glucose and C-reactive protein in middle-aged subjects
Aims C‐reactive protein (CRP), a marker of subclinical inflammation, predicts the occurrence of coronary heart disease in healthy subjects. Hyperglycaemia is known to stimulate the release of inflammatory cytokines from various cell types and can lead to the induction and secretion of acute‐phase r...
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| Published in: | Diabetic medicine 2004-01, Vol.21 (1), p.39-44 |
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| container_title | Diabetic medicine |
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| creator | Aronson, D. Bartha, P. Zinder, O. Kerner, A. Shitman, E. Markiewicz, W. Brook, G. J. Levy, Y. |
| description | Aims C‐reactive protein (CRP), a marker of subclinical inflammation, predicts the occurrence of coronary heart disease in healthy subjects. Hyperglycaemia is known to stimulate the release of inflammatory cytokines from various cell types and can lead to the induction and secretion of acute‐phase reactants by adipocytes. The aim of the present study was to determine the relation between glycaemic status and CRP in healthy subjects.
Methods We studied the relation of high‐sensitivity CRP to fasting glucose and other components of the metabolic syndrome in a population‐based cross‐sectional study (n = 1000; age 50 ± 9 years).
Results Plasma CRP levels increased continuously from the lowest quartile of normal fasting glucose level to impaired fasting glucose and to diabetes (ln CRP 0.47 ± 0.09, 0.95 ± 0.12, and 1.11 ± 0.13, respectively; Ptrend |
| doi_str_mv | 10.1046/j.1464-5491.2003.01084.x |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_80083950</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>80083950</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4994-1bf9f5e5f619fbe8b876a0934e2a49cc3e813d36f074c31cbe8265ea2e9899563</originalsourceid><addsrcrecordid>eNqNkM1u1DAUhS0EokPLKyBvYJdw_Zt4waIaSosoRar6I7GxHOd65CGTtHFCp29PwozabSVLtuTv-B5_hFAGOQOpP69zJrXMlDQs5wAiBwalzLevyOLp4jVZQCF5JqBgB-RdSmsAxo0wb8kBkwVoUHxBLo9T6nx0Q-xaWuHwgNjS4NIQ2xVdNaPvElLX1nSZ9ej8EP8iveu7AWNLp7WJdd1g5lZY0zRWa_RDOiJvgmsSvt_vh-T628nV8iw7_3X6fXl8nnlpjMxYFUxQqIJmJlRYVmWhHRghkTtpvBdYMlELHaZfeMH8hHCt0HE0pTFKi0Pyaffu1Od-xDTYTUwem8a12I3JlgClMAomsNyBvu9S6jHYuz5uXP9oGdjZp13bWZudtdnZp_3v026n6If9jLHaYP0c3AucgI97wCXvmtC71sf0zCnFOYO57Jcd9xAbfHxxAfv158l8mvLZLh_TgNunvOv_WF2IQtnbi1Or2fL3zY8zbrn4B3-7n7Y</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>80083950</pqid></control><display><type>article</type><title>Association between fasting glucose and C-reactive protein in middle-aged subjects</title><source>Wiley-Blackwell Read & Publish Collection</source><creator>Aronson, D. ; Bartha, P. ; Zinder, O. ; Kerner, A. ; Shitman, E. ; Markiewicz, W. ; Brook, G. J. ; Levy, Y.</creator><creatorcontrib>Aronson, D. ; Bartha, P. ; Zinder, O. ; Kerner, A. ; Shitman, E. ; Markiewicz, W. ; Brook, G. J. ; Levy, Y.</creatorcontrib><description>Aims C‐reactive protein (CRP), a marker of subclinical inflammation, predicts the occurrence of coronary heart disease in healthy subjects. Hyperglycaemia is known to stimulate the release of inflammatory cytokines from various cell types and can lead to the induction and secretion of acute‐phase reactants by adipocytes. The aim of the present study was to determine the relation between glycaemic status and CRP in healthy subjects.
Methods We studied the relation of high‐sensitivity CRP to fasting glucose and other components of the metabolic syndrome in a population‐based cross‐sectional study (n = 1000; age 50 ± 9 years).
Results Plasma CRP levels increased continuously from the lowest quartile of normal fasting glucose level to impaired fasting glucose and to diabetes (ln CRP 0.47 ± 0.09, 0.95 ± 0.12, and 1.11 ± 0.13, respectively; Ptrend < 0.0001). Increasing CRP with higher fasting glucose levels was apparent even among subjects with fasting glucose in the normal range (Ptrend = 0.039), and subjects with fasting glucose level in the upper quartile of normal fasting glucose had higher CRP levels compared with subjects in the lower quartile (P = 0.035). There was a positive crude correlation between CRP and smoking, post‐menopausal hormone use, body mass index, fasting glucose, triglycerides, hypertension, and uric acid (r = 0.11–0.36, P = 0.002–0.0001). A negative correlation was found between CRP and HDL‐cholesterol (r = 0.12, P < 0.0001) and physical activity (r = 0.11, P = 0.002). After adjustment for potential confounders in a stepwise multivariate linear regression model, fasting glucose remained significantly and independently related to CRP levels (correlation coefficient 0.06; 95% confidence interval 0.014–0.11, P = 0.011).
Conclusions Fasting glucose is significantly and positively associated with plasma CRP in middle‐aged subjects. CRP levels increase continuously across the spectrum of fasting glucose, beginning in the lowest quartile of normal fasting glucose. This finding suggests that a proinflammatory effect may contribute to the adverse cardiovascular outcome associated with diabetes, impaired fasting glucose, and increasing glucose levels within the normal range.</description><identifier>ISSN: 0742-3071</identifier><identifier>EISSN: 1464-5491</identifier><identifier>DOI: 10.1046/j.1464-5491.2003.01084.x</identifier><identifier>PMID: 14706052</identifier><identifier>CODEN: DIMEEV</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Biological and medical sciences ; Blood Glucose - analysis ; Body Mass Index ; C-reactive protein ; C-Reactive Protein - analysis ; Cholesterol, HDL - blood ; Cross-Sectional Studies ; Diabetes Mellitus - blood ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Fasting - blood ; Female ; glucose ; Hormone Replacement Therapy ; Humans ; inflammation ; insulin resistance syndrome ; Male ; Medical sciences ; Metabolic Syndrome - blood ; Middle Aged ; obesity ; Smoking ; Uric Acid - blood</subject><ispartof>Diabetic medicine, 2004-01, Vol.21 (1), p.39-44</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4994-1bf9f5e5f619fbe8b876a0934e2a49cc3e813d36f074c31cbe8265ea2e9899563</citedby><cites>FETCH-LOGICAL-c4994-1bf9f5e5f619fbe8b876a0934e2a49cc3e813d36f074c31cbe8265ea2e9899563</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15522106$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14706052$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aronson, D.</creatorcontrib><creatorcontrib>Bartha, P.</creatorcontrib><creatorcontrib>Zinder, O.</creatorcontrib><creatorcontrib>Kerner, A.</creatorcontrib><creatorcontrib>Shitman, E.</creatorcontrib><creatorcontrib>Markiewicz, W.</creatorcontrib><creatorcontrib>Brook, G. J.</creatorcontrib><creatorcontrib>Levy, Y.</creatorcontrib><title>Association between fasting glucose and C-reactive protein in middle-aged subjects</title><title>Diabetic medicine</title><addtitle>Diabet Med</addtitle><description>Aims C‐reactive protein (CRP), a marker of subclinical inflammation, predicts the occurrence of coronary heart disease in healthy subjects. Hyperglycaemia is known to stimulate the release of inflammatory cytokines from various cell types and can lead to the induction and secretion of acute‐phase reactants by adipocytes. The aim of the present study was to determine the relation between glycaemic status and CRP in healthy subjects.
Methods We studied the relation of high‐sensitivity CRP to fasting glucose and other components of the metabolic syndrome in a population‐based cross‐sectional study (n = 1000; age 50 ± 9 years).
Results Plasma CRP levels increased continuously from the lowest quartile of normal fasting glucose level to impaired fasting glucose and to diabetes (ln CRP 0.47 ± 0.09, 0.95 ± 0.12, and 1.11 ± 0.13, respectively; Ptrend < 0.0001). Increasing CRP with higher fasting glucose levels was apparent even among subjects with fasting glucose in the normal range (Ptrend = 0.039), and subjects with fasting glucose level in the upper quartile of normal fasting glucose had higher CRP levels compared with subjects in the lower quartile (P = 0.035). There was a positive crude correlation between CRP and smoking, post‐menopausal hormone use, body mass index, fasting glucose, triglycerides, hypertension, and uric acid (r = 0.11–0.36, P = 0.002–0.0001). A negative correlation was found between CRP and HDL‐cholesterol (r = 0.12, P < 0.0001) and physical activity (r = 0.11, P = 0.002). After adjustment for potential confounders in a stepwise multivariate linear regression model, fasting glucose remained significantly and independently related to CRP levels (correlation coefficient 0.06; 95% confidence interval 0.014–0.11, P = 0.011).
Conclusions Fasting glucose is significantly and positively associated with plasma CRP in middle‐aged subjects. CRP levels increase continuously across the spectrum of fasting glucose, beginning in the lowest quartile of normal fasting glucose. This finding suggests that a proinflammatory effect may contribute to the adverse cardiovascular outcome associated with diabetes, impaired fasting glucose, and increasing glucose levels within the normal range.</description><subject>Biological and medical sciences</subject><subject>Blood Glucose - analysis</subject><subject>Body Mass Index</subject><subject>C-reactive protein</subject><subject>C-Reactive Protein - analysis</subject><subject>Cholesterol, HDL - blood</subject><subject>Cross-Sectional Studies</subject><subject>Diabetes Mellitus - blood</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Fasting - blood</subject><subject>Female</subject><subject>glucose</subject><subject>Hormone Replacement Therapy</subject><subject>Humans</subject><subject>inflammation</subject><subject>insulin resistance syndrome</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic Syndrome - blood</subject><subject>Middle Aged</subject><subject>obesity</subject><subject>Smoking</subject><subject>Uric Acid - blood</subject><issn>0742-3071</issn><issn>1464-5491</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNqNkM1u1DAUhS0EokPLKyBvYJdw_Zt4waIaSosoRar6I7GxHOd65CGTtHFCp29PwozabSVLtuTv-B5_hFAGOQOpP69zJrXMlDQs5wAiBwalzLevyOLp4jVZQCF5JqBgB-RdSmsAxo0wb8kBkwVoUHxBLo9T6nx0Q-xaWuHwgNjS4NIQ2xVdNaPvElLX1nSZ9ej8EP8iveu7AWNLp7WJdd1g5lZY0zRWa_RDOiJvgmsSvt_vh-T628nV8iw7_3X6fXl8nnlpjMxYFUxQqIJmJlRYVmWhHRghkTtpvBdYMlELHaZfeMH8hHCt0HE0pTFKi0Pyaffu1Od-xDTYTUwem8a12I3JlgClMAomsNyBvu9S6jHYuz5uXP9oGdjZp13bWZudtdnZp_3v026n6If9jLHaYP0c3AucgI97wCXvmtC71sf0zCnFOYO57Jcd9xAbfHxxAfv158l8mvLZLh_TgNunvOv_WF2IQtnbi1Or2fL3zY8zbrn4B3-7n7Y</recordid><startdate>200401</startdate><enddate>200401</enddate><creator>Aronson, D.</creator><creator>Bartha, P.</creator><creator>Zinder, O.</creator><creator>Kerner, A.</creator><creator>Shitman, E.</creator><creator>Markiewicz, W.</creator><creator>Brook, G. J.</creator><creator>Levy, Y.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>200401</creationdate><title>Association between fasting glucose and C-reactive protein in middle-aged subjects</title><author>Aronson, D. ; Bartha, P. ; Zinder, O. ; Kerner, A. ; Shitman, E. ; Markiewicz, W. ; Brook, G. J. ; Levy, Y.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4994-1bf9f5e5f619fbe8b876a0934e2a49cc3e813d36f074c31cbe8265ea2e9899563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Biological and medical sciences</topic><topic>Blood Glucose - analysis</topic><topic>Body Mass Index</topic><topic>C-reactive protein</topic><topic>C-Reactive Protein - analysis</topic><topic>Cholesterol, HDL - blood</topic><topic>Cross-Sectional Studies</topic><topic>Diabetes Mellitus - blood</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Fasting - blood</topic><topic>Female</topic><topic>glucose</topic><topic>Hormone Replacement Therapy</topic><topic>Humans</topic><topic>inflammation</topic><topic>insulin resistance syndrome</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic Syndrome - blood</topic><topic>Middle Aged</topic><topic>obesity</topic><topic>Smoking</topic><topic>Uric Acid - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aronson, D.</creatorcontrib><creatorcontrib>Bartha, P.</creatorcontrib><creatorcontrib>Zinder, O.</creatorcontrib><creatorcontrib>Kerner, A.</creatorcontrib><creatorcontrib>Shitman, E.</creatorcontrib><creatorcontrib>Markiewicz, W.</creatorcontrib><creatorcontrib>Brook, G. J.</creatorcontrib><creatorcontrib>Levy, Y.</creatorcontrib><collection>Istex</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>MEDLINE - Academic</collection><jtitle>Diabetic medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aronson, D.</au><au>Bartha, P.</au><au>Zinder, O.</au><au>Kerner, A.</au><au>Shitman, E.</au><au>Markiewicz, W.</au><au>Brook, G. J.</au><au>Levy, Y.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association between fasting glucose and C-reactive protein in middle-aged subjects</atitle><jtitle>Diabetic medicine</jtitle><addtitle>Diabet Med</addtitle><date>2004-01</date><risdate>2004</risdate><volume>21</volume><issue>1</issue><spage>39</spage><epage>44</epage><pages>39-44</pages><issn>0742-3071</issn><eissn>1464-5491</eissn><coden>DIMEEV</coden><abstract>Aims C‐reactive protein (CRP), a marker of subclinical inflammation, predicts the occurrence of coronary heart disease in healthy subjects. Hyperglycaemia is known to stimulate the release of inflammatory cytokines from various cell types and can lead to the induction and secretion of acute‐phase reactants by adipocytes. The aim of the present study was to determine the relation between glycaemic status and CRP in healthy subjects.
Methods We studied the relation of high‐sensitivity CRP to fasting glucose and other components of the metabolic syndrome in a population‐based cross‐sectional study (n = 1000; age 50 ± 9 years).
Results Plasma CRP levels increased continuously from the lowest quartile of normal fasting glucose level to impaired fasting glucose and to diabetes (ln CRP 0.47 ± 0.09, 0.95 ± 0.12, and 1.11 ± 0.13, respectively; Ptrend < 0.0001). Increasing CRP with higher fasting glucose levels was apparent even among subjects with fasting glucose in the normal range (Ptrend = 0.039), and subjects with fasting glucose level in the upper quartile of normal fasting glucose had higher CRP levels compared with subjects in the lower quartile (P = 0.035). There was a positive crude correlation between CRP and smoking, post‐menopausal hormone use, body mass index, fasting glucose, triglycerides, hypertension, and uric acid (r = 0.11–0.36, P = 0.002–0.0001). A negative correlation was found between CRP and HDL‐cholesterol (r = 0.12, P < 0.0001) and physical activity (r = 0.11, P = 0.002). After adjustment for potential confounders in a stepwise multivariate linear regression model, fasting glucose remained significantly and independently related to CRP levels (correlation coefficient 0.06; 95% confidence interval 0.014–0.11, P = 0.011).
Conclusions Fasting glucose is significantly and positively associated with plasma CRP in middle‐aged subjects. CRP levels increase continuously across the spectrum of fasting glucose, beginning in the lowest quartile of normal fasting glucose. This finding suggests that a proinflammatory effect may contribute to the adverse cardiovascular outcome associated with diabetes, impaired fasting glucose, and increasing glucose levels within the normal range.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>14706052</pmid><doi>10.1046/j.1464-5491.2003.01084.x</doi><tpages>6</tpages></addata></record> |
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| ispartof | Diabetic medicine, 2004-01, Vol.21 (1), p.39-44 |
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| subjects | Biological and medical sciences Blood Glucose - analysis Body Mass Index C-reactive protein C-Reactive Protein - analysis Cholesterol, HDL - blood Cross-Sectional Studies Diabetes Mellitus - blood Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Fasting - blood Female glucose Hormone Replacement Therapy Humans inflammation insulin resistance syndrome Male Medical sciences Metabolic Syndrome - blood Middle Aged obesity Smoking Uric Acid - blood |
| title | Association between fasting glucose and C-reactive protein in middle-aged subjects |
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