Changes in protein turnover, IGF-I and IGF binding proteins in children with cancer
Changes in insulin‐like growth factor‐I (IGF‐I) and insulin‐like growth factor binding proteins (IGFBPs) were correlated with protein synthesis and breakdown using [1‐ 13C]leucine before chemotherapy and during subsequent febrile neutropenia (FN) in eight children with cancer, aged 6.3–17.5 y. IGF‐I...
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| Veröffentlicht in: | Acta Paediatrica 1998-01, Vol.87 (1), p.54-60 |
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| creator | Attard-Montalto, SP Camacho-Hübner, C Cotterill, AM D'Souza-Li, L Daley, S Bartlett, K Halliday, D Eden, OB |
| description | Changes in insulin‐like growth factor‐I (IGF‐I) and insulin‐like growth factor binding proteins (IGFBPs) were correlated with protein synthesis and breakdown using [1‐ 13C]leucine before chemotherapy and during subsequent febrile neutropenia (FN) in eight children with cancer, aged 6.3–17.5 y. IGF‐I levels were similar to age‐matched controls before chemotherapy (mean ±SEM: 250 ±28 and 228 ±22 μg l‐1, respectively). During FN, IGF‐I fell to 156 ±22 /ng l ‐1(p= 0:02), and rose to 276 ±27 μ g l ‐1 with recovery at 6 months (p = 0:004). Similarly, IGFBP‐3 decreased from 4.0 ±0.2mgl‐1 before chemotherapy to 3.0 ±0.3 mgl‐1 during FN (p= 0:01), and returned to 4.1 ±0.2mgl ‐1 at 6 months (p= 0:01). IGF‐I correlated with IGFBP‐3 (r=+0:7, p |
| doi_str_mv | 10.1111/j.1651-2227.1998.tb01386.x |
| format | Article |
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IGF‐I levels were similar to age‐matched controls before chemotherapy (mean ±SEM: 250 ±28 and 228 ±22 μg l‐1, respectively). During FN, IGF‐I fell to 156 ±22 /ng l ‐1(p= 0:02), and rose to 276 ±27 μ g l ‐1 with recovery at 6 months (p = 0:004). Similarly, IGFBP‐3 decreased from 4.0 ±0.2mgl‐1 before chemotherapy to 3.0 ±0.3 mgl‐1 during FN (p= 0:01), and returned to 4.1 ±0.2mgl ‐1 at 6 months (p= 0:01). IGF‐I correlated with IGFBP‐3 (r=+0:7, p <0:001). Scanning densitometry showed a decrease in IGFBP‐3 from 94 to 54% during FN, when the presence of IGFBP‐3 protease activity was observed. Compared with normal human serum, IGFBP‐2 was elevated throughout the study. IGFBP‐1 increased from 14.6 ±3.5 to 30.6 ±2.8/ngl‐1 (p = 0:004), whereas serum insulin decreased from 26.5 ±6.8 to 7.8 ±0.8 mUl‐1 (p= 0:03) before and during FN, respectively. Whilst IGF‐I and IGFBP‐3 fell, daytime growth hormone increased from 3.3 ±0.6 to 6.7±0.8mUl ‐1 (p= 0:01), and cortisol from 197 ±48 to 594±98nmoll ‐1 (p = 0:005). Albumin decreased from 47 ±2 to 38 ±2gl‐1 (p= 0:004) and improved to 47 ±2gl‐1 with recovery (p= 0:003). Protein synthesis increased from 4.5 ±0.4 to 5.0 ±0.6gkg‐1 d‐1 before chemotherapy and during FN, while protein breakdown rose from 5.4 ±0.4 to 6.3 ±0.4kg‐1d‐1. Increasing protein breakdown was related to falling IGF‐I and IGFBP‐3 levels. Modification of IGFBP‐3 by circulating proteolytic activity may alter IGF bioavailability, allowing protein synthesis to increase during periods of severe catabolic stress.</description><identifier>ISSN: 0803-5253</identifier><identifier>EISSN: 1651-2227</identifier><identifier>DOI: 10.1111/j.1651-2227.1998.tb01386.x</identifier><identifier>PMID: 9510448</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adolescent ; Anthropometry ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Biological and medical sciences ; Cachexia - etiology ; Cachexia - metabolism ; Chemotherapy-cachexia ; Child ; Female ; Humans ; IGF-I ; IGFBPs ; Insulin - biosynthesis ; Insulin - metabolism ; Insulin-Like Growth Factor Binding Proteins - biosynthesis ; Insulin-Like Growth Factor Binding Proteins - metabolism ; Insulin-Like Growth Factor I - biosynthesis ; Insulin-Like Growth Factor I - metabolism ; Lymphoma, Non-Hodgkin - complications ; Lymphoma, Non-Hodgkin - drug therapy ; Lymphoma, Non-Hodgkin - metabolism ; Male ; Medical sciences ; Multiple tumors. Solid tumors. Tumors in childhood (general aspects) ; Muscle Proteins - metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - complications ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism ; Prognosis ; protein turnover ; Radioimmunoassay ; Reference Values ; Regression Analysis ; Rhabdomyosarcoma, Alveolar - complications ; Rhabdomyosarcoma, Alveolar - drug therapy ; Rhabdomyosarcoma, Alveolar - metabolism ; Tumors</subject><ispartof>Acta Paediatrica, 1998-01, Vol.87 (1), p.54-60</ispartof><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2824-2bf7275e89a33340905738890ecea7ea542559d66d3990db7fa816a90b5ba4da3</citedby><cites>FETCH-LOGICAL-c2824-2bf7275e89a33340905738890ecea7ea542559d66d3990db7fa816a90b5ba4da3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1651-2227.1998.tb01386.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1651-2227.1998.tb01386.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,4009,27902,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2155946$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9510448$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Attard-Montalto, SP</creatorcontrib><creatorcontrib>Camacho-Hübner, C</creatorcontrib><creatorcontrib>Cotterill, AM</creatorcontrib><creatorcontrib>D'Souza-Li, L</creatorcontrib><creatorcontrib>Daley, S</creatorcontrib><creatorcontrib>Bartlett, K</creatorcontrib><creatorcontrib>Halliday, D</creatorcontrib><creatorcontrib>Eden, OB</creatorcontrib><title>Changes in protein turnover, IGF-I and IGF binding proteins in children with cancer</title><title>Acta Paediatrica</title><addtitle>Acta Paediatr</addtitle><description>Changes in insulin‐like growth factor‐I (IGF‐I) and insulin‐like growth factor binding proteins (IGFBPs) were correlated with protein synthesis and breakdown using [1‐ 13C]leucine before chemotherapy and during subsequent febrile neutropenia (FN) in eight children with cancer, aged 6.3–17.5 y. IGF‐I levels were similar to age‐matched controls before chemotherapy (mean ±SEM: 250 ±28 and 228 ±22 μg l‐1, respectively). During FN, IGF‐I fell to 156 ±22 /ng l ‐1(p= 0:02), and rose to 276 ±27 μ g l ‐1 with recovery at 6 months (p = 0:004). Similarly, IGFBP‐3 decreased from 4.0 ±0.2mgl‐1 before chemotherapy to 3.0 ±0.3 mgl‐1 during FN (p= 0:01), and returned to 4.1 ±0.2mgl ‐1 at 6 months (p= 0:01). IGF‐I correlated with IGFBP‐3 (r=+0:7, p <0:001). Scanning densitometry showed a decrease in IGFBP‐3 from 94 to 54% during FN, when the presence of IGFBP‐3 protease activity was observed. Compared with normal human serum, IGFBP‐2 was elevated throughout the study. IGFBP‐1 increased from 14.6 ±3.5 to 30.6 ±2.8/ngl‐1 (p = 0:004), whereas serum insulin decreased from 26.5 ±6.8 to 7.8 ±0.8 mUl‐1 (p= 0:03) before and during FN, respectively. Whilst IGF‐I and IGFBP‐3 fell, daytime growth hormone increased from 3.3 ±0.6 to 6.7±0.8mUl ‐1 (p= 0:01), and cortisol from 197 ±48 to 594±98nmoll ‐1 (p = 0:005). Albumin decreased from 47 ±2 to 38 ±2gl‐1 (p= 0:004) and improved to 47 ±2gl‐1 with recovery (p= 0:003). Protein synthesis increased from 4.5 ±0.4 to 5.0 ±0.6gkg‐1 d‐1 before chemotherapy and during FN, while protein breakdown rose from 5.4 ±0.4 to 6.3 ±0.4kg‐1d‐1. Increasing protein breakdown was related to falling IGF‐I and IGFBP‐3 levels. Modification of IGFBP‐3 by circulating proteolytic activity may alter IGF bioavailability, allowing protein synthesis to increase during periods of severe catabolic stress.</description><subject>Adolescent</subject><subject>Anthropometry</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Cachexia - etiology</subject><subject>Cachexia - metabolism</subject><subject>Chemotherapy-cachexia</subject><subject>Child</subject><subject>Female</subject><subject>Humans</subject><subject>IGF-I</subject><subject>IGFBPs</subject><subject>Insulin - biosynthesis</subject><subject>Insulin - metabolism</subject><subject>Insulin-Like Growth Factor Binding Proteins - biosynthesis</subject><subject>Insulin-Like Growth Factor Binding Proteins - metabolism</subject><subject>Insulin-Like Growth Factor I - biosynthesis</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>Lymphoma, Non-Hodgkin - complications</subject><subject>Lymphoma, Non-Hodgkin - drug therapy</subject><subject>Lymphoma, Non-Hodgkin - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</subject><subject>Muscle Proteins - metabolism</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - complications</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism</subject><subject>Prognosis</subject><subject>protein turnover</subject><subject>Radioimmunoassay</subject><subject>Reference Values</subject><subject>Regression Analysis</subject><subject>Rhabdomyosarcoma, Alveolar - complications</subject><subject>Rhabdomyosarcoma, Alveolar - drug therapy</subject><subject>Rhabdomyosarcoma, Alveolar - metabolism</subject><subject>Tumors</subject><issn>0803-5253</issn><issn>1651-2227</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkF1P2zAUhq1piBXGT5gUoWlXJPj7Y9IuqgpKRbVNG9Ok3VhO4lCX1AU7hfLvcWjo_XxzLJ338Tl-ADhFsEDpnC8LxBnKMcaiQErJoishIpIX23dgtG-9ByMoIckZZuQDOIpxCSEmivJDcKgYgpTKEfg9WRh_a2PmfHYf1p1NtdsEv3604SybTS_zWWZ83d-y0vna-du33CtTLVxbB-uzJ9ctssr4yoaP4KAxbbQnQz0Gfy4vbiZX-fzHdDYZz_MKS0xzXDYCC2alMoQQChVkgkipoK2sEdYwihlTNec1UQrWpWiMRNwoWLLS0NqQY_Bl925a6GFjY6dXLla2bY23603UQgnCCUYp-HUXrMI6xmAbfR_cyoRnjaDujeql7rXpXpvujerBqN4m-NMwZVOubL1HB4Wp_3nom1iZtgnJgYv7GEbpE5Sn2Ldd7Mm19vk_FtDjn2NGE5_veBc7u93zJtxpLohg-u_3qab_JlfX9Hquf5EX8ZGgGg</recordid><startdate>199801</startdate><enddate>199801</enddate><creator>Attard-Montalto, SP</creator><creator>Camacho-Hübner, C</creator><creator>Cotterill, AM</creator><creator>D'Souza-Li, L</creator><creator>Daley, S</creator><creator>Bartlett, K</creator><creator>Halliday, D</creator><creator>Eden, OB</creator><general>Blackwell Publishing 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>199801</creationdate><title>Changes in protein turnover, IGF-I and IGF binding proteins in children with cancer</title><author>Attard-Montalto, SP ; Camacho-Hübner, C ; Cotterill, AM ; D'Souza-Li, L ; Daley, S ; Bartlett, K ; Halliday, D ; Eden, OB</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2824-2bf7275e89a33340905738890ecea7ea542559d66d3990db7fa816a90b5ba4da3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adolescent</topic><topic>Anthropometry</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Cachexia - etiology</topic><topic>Cachexia - metabolism</topic><topic>Chemotherapy-cachexia</topic><topic>Child</topic><topic>Female</topic><topic>Humans</topic><topic>IGF-I</topic><topic>IGFBPs</topic><topic>Insulin - biosynthesis</topic><topic>Insulin - metabolism</topic><topic>Insulin-Like Growth Factor Binding Proteins - biosynthesis</topic><topic>Insulin-Like Growth Factor Binding Proteins - metabolism</topic><topic>Insulin-Like Growth Factor I - biosynthesis</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>Lymphoma, Non-Hodgkin - complications</topic><topic>Lymphoma, Non-Hodgkin - drug therapy</topic><topic>Lymphoma, Non-Hodgkin - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</topic><topic>Muscle Proteins - metabolism</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - complications</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism</topic><topic>Prognosis</topic><topic>protein turnover</topic><topic>Radioimmunoassay</topic><topic>Reference Values</topic><topic>Regression Analysis</topic><topic>Rhabdomyosarcoma, Alveolar - complications</topic><topic>Rhabdomyosarcoma, Alveolar - drug therapy</topic><topic>Rhabdomyosarcoma, Alveolar - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Attard-Montalto, SP</creatorcontrib><creatorcontrib>Camacho-Hübner, C</creatorcontrib><creatorcontrib>Cotterill, AM</creatorcontrib><creatorcontrib>D'Souza-Li, L</creatorcontrib><creatorcontrib>Daley, S</creatorcontrib><creatorcontrib>Bartlett, K</creatorcontrib><creatorcontrib>Halliday, D</creatorcontrib><creatorcontrib>Eden, OB</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>Acta Paediatrica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Attard-Montalto, SP</au><au>Camacho-Hübner, C</au><au>Cotterill, AM</au><au>D'Souza-Li, L</au><au>Daley, S</au><au>Bartlett, K</au><au>Halliday, D</au><au>Eden, OB</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in protein turnover, IGF-I and IGF binding proteins in children with cancer</atitle><jtitle>Acta Paediatrica</jtitle><addtitle>Acta Paediatr</addtitle><date>1998-01</date><risdate>1998</risdate><volume>87</volume><issue>1</issue><spage>54</spage><epage>60</epage><pages>54-60</pages><issn>0803-5253</issn><eissn>1651-2227</eissn><abstract>Changes in insulin‐like growth factor‐I (IGF‐I) and insulin‐like growth factor binding proteins (IGFBPs) were correlated with protein synthesis and breakdown using [1‐ 13C]leucine before chemotherapy and during subsequent febrile neutropenia (FN) in eight children with cancer, aged 6.3–17.5 y. IGF‐I levels were similar to age‐matched controls before chemotherapy (mean ±SEM: 250 ±28 and 228 ±22 μg l‐1, respectively). During FN, IGF‐I fell to 156 ±22 /ng l ‐1(p= 0:02), and rose to 276 ±27 μ g l ‐1 with recovery at 6 months (p = 0:004). Similarly, IGFBP‐3 decreased from 4.0 ±0.2mgl‐1 before chemotherapy to 3.0 ±0.3 mgl‐1 during FN (p= 0:01), and returned to 4.1 ±0.2mgl ‐1 at 6 months (p= 0:01). IGF‐I correlated with IGFBP‐3 (r=+0:7, p <0:001). Scanning densitometry showed a decrease in IGFBP‐3 from 94 to 54% during FN, when the presence of IGFBP‐3 protease activity was observed. Compared with normal human serum, IGFBP‐2 was elevated throughout the study. IGFBP‐1 increased from 14.6 ±3.5 to 30.6 ±2.8/ngl‐1 (p = 0:004), whereas serum insulin decreased from 26.5 ±6.8 to 7.8 ±0.8 mUl‐1 (p= 0:03) before and during FN, respectively. Whilst IGF‐I and IGFBP‐3 fell, daytime growth hormone increased from 3.3 ±0.6 to 6.7±0.8mUl ‐1 (p= 0:01), and cortisol from 197 ±48 to 594±98nmoll ‐1 (p = 0:005). Albumin decreased from 47 ±2 to 38 ±2gl‐1 (p= 0:004) and improved to 47 ±2gl‐1 with recovery (p= 0:003). Protein synthesis increased from 4.5 ±0.4 to 5.0 ±0.6gkg‐1 d‐1 before chemotherapy and during FN, while protein breakdown rose from 5.4 ±0.4 to 6.3 ±0.4kg‐1d‐1. Increasing protein breakdown was related to falling IGF‐I and IGFBP‐3 levels. Modification of IGFBP‐3 by circulating proteolytic activity may alter IGF bioavailability, allowing protein synthesis to increase during periods of severe catabolic stress.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>9510448</pmid><doi>10.1111/j.1651-2227.1998.tb01386.x</doi><tpages>7</tpages></addata></record> |
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| subjects | Adolescent Anthropometry Antineoplastic Combined Chemotherapy Protocols - therapeutic use Biological and medical sciences Cachexia - etiology Cachexia - metabolism Chemotherapy-cachexia Child Female Humans IGF-I IGFBPs Insulin - biosynthesis Insulin - metabolism Insulin-Like Growth Factor Binding Proteins - biosynthesis Insulin-Like Growth Factor Binding Proteins - metabolism Insulin-Like Growth Factor I - biosynthesis Insulin-Like Growth Factor I - metabolism Lymphoma, Non-Hodgkin - complications Lymphoma, Non-Hodgkin - drug therapy Lymphoma, Non-Hodgkin - metabolism Male Medical sciences Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Muscle Proteins - metabolism Precursor Cell Lymphoblastic Leukemia-Lymphoma - complications Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism Prognosis protein turnover Radioimmunoassay Reference Values Regression Analysis Rhabdomyosarcoma, Alveolar - complications Rhabdomyosarcoma, Alveolar - drug therapy Rhabdomyosarcoma, Alveolar - metabolism Tumors |
| title | Changes in protein turnover, IGF-I and IGF binding proteins in children with cancer |
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