Soluble leptin receptors and serum leptin in end-stage renal disease: relationship with inflammation and body composition

Background Elevated serum leptin (S‐leptin) levels have been reported in patients with end‐stage renal disease (ESRD). Apart from the decreased glomerular filtration rate (GFR), body composition and inflammation may affect leptin levels in ESRD. Leptin circulates both free of and bound to soluble le...

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Veröffentlicht in:European journal of clinical investigation 2002-11, Vol.32 (11), p.811-817
Hauptverfasser: Pecoits-Filho, R., Nordfors, L., Heimbürger, O., Lindholm, B., Anderstam, B., Marchlewska, A., Stenvinkel, P.
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container_issue 11
container_start_page 811
container_title European journal of clinical investigation
container_volume 32
creator Pecoits-Filho, R.
Nordfors, L.
Heimbürger, O.
Lindholm, B.
Anderstam, B.
Marchlewska, A.
Stenvinkel, P.
description Background Elevated serum leptin (S‐leptin) levels have been reported in patients with end‐stage renal disease (ESRD). Apart from the decreased glomerular filtration rate (GFR), body composition and inflammation may affect leptin levels in ESRD. Leptin circulates both free of and bound to soluble leptin receptors (sOB‐R), which are the main determinants of leptin activity and have not been described in ESRD until now. Design To analyze the association between S‐leptin, sOB‐R, and inflammation and body composition, we studied 149 (62% males) normal weight (BMI 24·7 ± 0·4 kg m−2) ESRD patients (51 ± 1 years old) shortly before the start of dialysis (GFR 7·0 ± 0·2 mL min−1). sOB‐R and plasma interleukin‐6 (IL‐6; n= 113) levels were evaluated using ELISA, S‐leptin using RIA, and body composition was assessed by X‐ray absorptiometry (n = 139). Forty‐one healthy subjects age (51 ± 1 years), BMI (23·6 ± 0·5 kg m−2) and gender‐matched (59% males) were used as controls. Results Median S‐leptin was higher in the ESRD patients (10·0 ng mL−1) compared with the controls (3·9 ng mL−1) (P 
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Apart from the decreased glomerular filtration rate (GFR), body composition and inflammation may affect leptin levels in ESRD. Leptin circulates both free of and bound to soluble leptin receptors (sOB‐R), which are the main determinants of leptin activity and have not been described in ESRD until now. Design To analyze the association between S‐leptin, sOB‐R, and inflammation and body composition, we studied 149 (62% males) normal weight (BMI 24·7 ± 0·4 kg m−2) ESRD patients (51 ± 1 years old) shortly before the start of dialysis (GFR 7·0 ± 0·2 mL min−1). sOB‐R and plasma interleukin‐6 (IL‐6; n= 113) levels were evaluated using ELISA, S‐leptin using RIA, and body composition was assessed by X‐ray absorptiometry (n = 139). Forty‐one healthy subjects age (51 ± 1 years), BMI (23·6 ± 0·5 kg m−2) and gender‐matched (59% males) were used as controls. Results Median S‐leptin was higher in the ESRD patients (10·0 ng mL−1) compared with the controls (3·9 ng mL−1) (P < 0·001). The median sOB‐R did not differ significantly between the ESRD patients (44 U mL−1) and the controls (37 U mL−1). Thus, the sOB‐R/S‐leptin ratio was lower in the ESRD patients (9·5 ± 1·2 vs. 12·3 ± 1·8; P < 0·01) than the controls. A negative correlation was observed between S‐leptin and sOB‐R (Rho = −0·42; P < 0·0001) in the ESRD patients, a positive correlation was observed between lean body mass and the sOB‐R/S‐leptin ratio (Rho = 0·33, P = 0·0001) whereas fat mass was negatively correlated to both sOB‐R (Rho = −0·26, P = 0·002), and the sOB‐R/S‐leptin ratio (Rho = −0·62, P < 0·0001). Positive correlations were observed between IL‐6 and S‐leptin (Rho = 0·19; P < 0·05) and weak but significant body fat mass (Rho = 0·20; P < 0·05), respectively. Conclusions This study demonstrates that despite markedly elevated S‐leptin levels in the ESRD patients, sOB‐R did not differ from the controls. In view of the anorexigenic and pro‐atherogenic effects of leptin, further elucidation of the consequences of free bioactive leptin in the development of complications such as malnutrition and cardiovascular disease in ESRD patients is required.]]></description><identifier>ISSN: 0014-2972</identifier><identifier>EISSN: 1365-2362</identifier><identifier>DOI: 10.1046/j.1365-2362.2002.01063.x</identifier><identifier>PMID: 12423321</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Biological and medical sciences ; Body Composition ; Case-Control Studies ; Diabetes Mellitus - blood ; Diabetes Mellitus - immunology ; Diabetes Mellitus - metabolism ; end-stage renal disease ; Female ; Humans ; inflammation ; Interleukin-6 - blood ; Kidney Failure, Chronic - blood ; Kidney Failure, Chronic - immunology ; Kidney Failure, Chronic - metabolism ; leptin ; Leptin - blood ; Male ; Medical sciences ; Middle Aged ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Prospective Studies ; Receptors, Cell Surface - blood ; Receptors, Leptin ; Renal failure ; soluble leptin receptors ; Statistics, Nonparametric</subject><ispartof>European journal of clinical investigation, 2002-11, Vol.32 (11), p.811-817</ispartof><rights>2003 INIST-CNRS</rights><rights>Copyright Blackwell Scientific Publications Ltd. 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Apart from the decreased glomerular filtration rate (GFR), body composition and inflammation may affect leptin levels in ESRD. Leptin circulates both free of and bound to soluble leptin receptors (sOB‐R), which are the main determinants of leptin activity and have not been described in ESRD until now. Design To analyze the association between S‐leptin, sOB‐R, and inflammation and body composition, we studied 149 (62% males) normal weight (BMI 24·7 ± 0·4 kg m−2) ESRD patients (51 ± 1 years old) shortly before the start of dialysis (GFR 7·0 ± 0·2 mL min−1). sOB‐R and plasma interleukin‐6 (IL‐6; n= 113) levels were evaluated using ELISA, S‐leptin using RIA, and body composition was assessed by X‐ray absorptiometry (n = 139). Forty‐one healthy subjects age (51 ± 1 years), BMI (23·6 ± 0·5 kg m−2) and gender‐matched (59% males) were used as controls. Results Median S‐leptin was higher in the ESRD patients (10·0 ng mL−1) compared with the controls (3·9 ng mL−1) (P < 0·001). The median sOB‐R did not differ significantly between the ESRD patients (44 U mL−1) and the controls (37 U mL−1). Thus, the sOB‐R/S‐leptin ratio was lower in the ESRD patients (9·5 ± 1·2 vs. 12·3 ± 1·8; P < 0·01) than the controls. A negative correlation was observed between S‐leptin and sOB‐R (Rho = −0·42; P < 0·0001) in the ESRD patients, a positive correlation was observed between lean body mass and the sOB‐R/S‐leptin ratio (Rho = 0·33, P = 0·0001) whereas fat mass was negatively correlated to both sOB‐R (Rho = −0·26, P = 0·002), and the sOB‐R/S‐leptin ratio (Rho = −0·62, P < 0·0001). Positive correlations were observed between IL‐6 and S‐leptin (Rho = 0·19; P < 0·05) and weak but significant body fat mass (Rho = 0·20; P < 0·05), respectively. Conclusions This study demonstrates that despite markedly elevated S‐leptin levels in the ESRD patients, sOB‐R did not differ from the controls. In view of the anorexigenic and pro‐atherogenic effects of leptin, further elucidation of the consequences of free bioactive leptin in the development of complications such as malnutrition and cardiovascular disease in ESRD patients is required.]]></description><subject>Biological and medical sciences</subject><subject>Body Composition</subject><subject>Case-Control Studies</subject><subject>Diabetes Mellitus - blood</subject><subject>Diabetes Mellitus - immunology</subject><subject>Diabetes Mellitus - metabolism</subject><subject>end-stage renal disease</subject><subject>Female</subject><subject>Humans</subject><subject>inflammation</subject><subject>Interleukin-6 - blood</subject><subject>Kidney Failure, Chronic - blood</subject><subject>Kidney Failure, Chronic - immunology</subject><subject>Kidney Failure, Chronic - metabolism</subject><subject>leptin</subject><subject>Leptin - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Prospective Studies</subject><subject>Receptors, Cell Surface - blood</subject><subject>Receptors, Leptin</subject><subject>Renal failure</subject><subject>soluble leptin receptors</subject><subject>Statistics, Nonparametric</subject><issn>0014-2972</issn><issn>1365-2362</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkd-L1DAQx4so3nr6L0gR9K1rMmnTVPBBlvsFpz6c4GNI2qmXvbSpScvu_vemu-su-CQEMpn5fCfDfJMkpWRJSc4_rpeU8SIDxmEJhMCSUMLZcvssWZwKz5MFITTPoCrhInkVwpoQIiiDl8kFhRwYA7pIdg_OTtpianEYTZ96rGPgfEhV36QB_dT9LcWDfZOFUf3CyPXKpo0JqAJ-ik-rRuP68GiGdGPGx0i3VnXdPrvvpV2zS2vXDS6YOfk6edEqG_DN8b5MHq6vfqxus_vvN3erL_dZXUDJsrYglOlWI4MWRV2XTcGhKAXXCmOpUoIXVGhUggLXWrQNMGRtrqDJmWaXSXboGjY4TFoO3nTK76RTRh5TTzFCWVRAgEf-w4EfvPs9YRhlZ0KN1qoe3RRkCZwLkbMIvvsHXLvJx6UESauKAuFQRUgcoNq7EDy2p_8pkbOTci1nw-RsmJydlHsn5TZK3x77T7rD5iw8WheB90dAhVrZ1qu-NuHM5YRyQuZBPx-4jbG4--8B5NXqbo7OGzRhxO1Jr_yT5CUrC_nz2438ylklbksqr9kfL4HKUQ</recordid><startdate>200211</startdate><enddate>200211</enddate><creator>Pecoits-Filho, R.</creator><creator>Nordfors, L.</creator><creator>Heimbürger, O.</creator><creator>Lindholm, B.</creator><creator>Anderstam, B.</creator><creator>Marchlewska, A.</creator><creator>Stenvinkel, P.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Blackwell Publishing Ltd</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>7QO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>200211</creationdate><title>Soluble leptin receptors and serum leptin in end-stage renal disease: relationship with inflammation and body composition</title><author>Pecoits-Filho, R. ; Nordfors, L. ; Heimbürger, O. ; Lindholm, B. ; Anderstam, B. ; Marchlewska, A. ; Stenvinkel, P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5273-f5013bfbe32fe8cc7d5625786bae5019a86518bea8126bb8fd23e3f4a2d43b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Biological and medical sciences</topic><topic>Body Composition</topic><topic>Case-Control Studies</topic><topic>Diabetes Mellitus - blood</topic><topic>Diabetes Mellitus - immunology</topic><topic>Diabetes Mellitus - metabolism</topic><topic>end-stage renal disease</topic><topic>Female</topic><topic>Humans</topic><topic>inflammation</topic><topic>Interleukin-6 - blood</topic><topic>Kidney Failure, Chronic - blood</topic><topic>Kidney Failure, Chronic - immunology</topic><topic>Kidney Failure, Chronic - metabolism</topic><topic>leptin</topic><topic>Leptin - blood</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Prospective Studies</topic><topic>Receptors, Cell Surface - blood</topic><topic>Receptors, Leptin</topic><topic>Renal failure</topic><topic>soluble leptin receptors</topic><topic>Statistics, Nonparametric</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pecoits-Filho, R.</creatorcontrib><creatorcontrib>Nordfors, L.</creatorcontrib><creatorcontrib>Heimbürger, O.</creatorcontrib><creatorcontrib>Lindholm, B.</creatorcontrib><creatorcontrib>Anderstam, B.</creatorcontrib><creatorcontrib>Marchlewska, A.</creatorcontrib><creatorcontrib>Stenvinkel, P.</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>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>European journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pecoits-Filho, R.</au><au>Nordfors, L.</au><au>Heimbürger, O.</au><au>Lindholm, B.</au><au>Anderstam, B.</au><au>Marchlewska, A.</au><au>Stenvinkel, P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Soluble leptin receptors and serum leptin in end-stage renal disease: relationship with inflammation and body composition</atitle><jtitle>European journal of clinical investigation</jtitle><addtitle>Eur J Clin Invest</addtitle><date>2002-11</date><risdate>2002</risdate><volume>32</volume><issue>11</issue><spage>811</spage><epage>817</epage><pages>811-817</pages><issn>0014-2972</issn><eissn>1365-2362</eissn><abstract><![CDATA[Background Elevated serum leptin (S‐leptin) levels have been reported in patients with end‐stage renal disease (ESRD). Apart from the decreased glomerular filtration rate (GFR), body composition and inflammation may affect leptin levels in ESRD. Leptin circulates both free of and bound to soluble leptin receptors (sOB‐R), which are the main determinants of leptin activity and have not been described in ESRD until now. Design To analyze the association between S‐leptin, sOB‐R, and inflammation and body composition, we studied 149 (62% males) normal weight (BMI 24·7 ± 0·4 kg m−2) ESRD patients (51 ± 1 years old) shortly before the start of dialysis (GFR 7·0 ± 0·2 mL min−1). sOB‐R and plasma interleukin‐6 (IL‐6; n= 113) levels were evaluated using ELISA, S‐leptin using RIA, and body composition was assessed by X‐ray absorptiometry (n = 139). Forty‐one healthy subjects age (51 ± 1 years), BMI (23·6 ± 0·5 kg m−2) and gender‐matched (59% males) were used as controls. Results Median S‐leptin was higher in the ESRD patients (10·0 ng mL−1) compared with the controls (3·9 ng mL−1) (P < 0·001). The median sOB‐R did not differ significantly between the ESRD patients (44 U mL−1) and the controls (37 U mL−1). Thus, the sOB‐R/S‐leptin ratio was lower in the ESRD patients (9·5 ± 1·2 vs. 12·3 ± 1·8; P < 0·01) than the controls. A negative correlation was observed between S‐leptin and sOB‐R (Rho = −0·42; P < 0·0001) in the ESRD patients, a positive correlation was observed between lean body mass and the sOB‐R/S‐leptin ratio (Rho = 0·33, P = 0·0001) whereas fat mass was negatively correlated to both sOB‐R (Rho = −0·26, P = 0·002), and the sOB‐R/S‐leptin ratio (Rho = −0·62, P < 0·0001). Positive correlations were observed between IL‐6 and S‐leptin (Rho = 0·19; P < 0·05) and weak but significant body fat mass (Rho = 0·20; P < 0·05), respectively. Conclusions This study demonstrates that despite markedly elevated S‐leptin levels in the ESRD patients, sOB‐R did not differ from the controls. In view of the anorexigenic and pro‐atherogenic effects of leptin, further elucidation of the consequences of free bioactive leptin in the development of complications such as malnutrition and cardiovascular disease in ESRD patients is required.]]></abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>12423321</pmid><doi>10.1046/j.1365-2362.2002.01063.x</doi><tpages>7</tpages></addata></record>
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subjects Biological and medical sciences
Body Composition
Case-Control Studies
Diabetes Mellitus - blood
Diabetes Mellitus - immunology
Diabetes Mellitus - metabolism
end-stage renal disease
Female
Humans
inflammation
Interleukin-6 - blood
Kidney Failure, Chronic - blood
Kidney Failure, Chronic - immunology
Kidney Failure, Chronic - metabolism
leptin
Leptin - blood
Male
Medical sciences
Middle Aged
Nephrology. Urinary tract diseases
Nephropathies. Renovascular diseases. Renal failure
Prospective Studies
Receptors, Cell Surface - blood
Receptors, Leptin
Renal failure
soluble leptin receptors
Statistics, Nonparametric
title Soluble leptin receptors and serum leptin in end-stage renal disease: relationship with inflammation and body composition
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