Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model.

Rats bearing the Yoshida AH-130 ascites hepatoma showed enhanced fractional rates of protein degradation in gastrocnemius muscle, heart, and liver, while fractional synthesis rates were similar to those in non-tumor bearing rats. This hypercatabolic pattern was associated with marked perturbations o...

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Autores: Costelli, Paola, Carbó Carbó, Neus, Tessitore, Luciana, Bagby, Gregory J., López-Soriano, Francisco J., Argilés Huguet, Josep Ma., Baccino, Francesco M.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:1993
País:España
Institución:Universidad de Barcelona
Repositorio:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/8263
Acceso en línea:https://hdl.handle.net/2445/8263
Access Level:acceso abierto
Palabra clave:Tumors
Necrosi
Músculs
Tumor necrosis factor
Skeletal muscle
Protein turnover
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spelling Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model.Costelli, PaolaCarbó Carbó, NeusTessitore, LucianaBagby, Gregory J.López-Soriano, Francisco J.Argilés Huguet, Josep Ma.Baccino, Francesco M.TumorsNecrosiMúsculsTumor necrosis factorSkeletal muscleProtein turnoverRats bearing the Yoshida AH-130 ascites hepatoma showed enhanced fractional rates of protein degradation in gastrocnemius muscle, heart, and liver, while fractional synthesis rates were similar to those in non-tumor bearing rats. This hypercatabolic pattern was associated with marked perturbations of the hormonal homeostasis and presence of tumor necrosis factor in the circulation. The daily administration of a goat anti-murine TNF IgG to tumor-bearing rats decreased protein degradation rates in skeletal muscle, heart, and liver as compared with tumor-bearing rats receiving a nonimmune goat IgG. The anti-TNF treatment was also effective in attenuating early perturbations in insulin and corticosterone homeostasis. Although these results suggest that tumor necrosis factor plays a significant role in mediating the changes in protein turnover and hormone levels elicited by tumor growth, the inability of such treatment to prevent a reduction in body weight implies that other mediators or tumor-related events were also involved.American Society for Clinical Investigation1993info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://hdl.handle.net/2445/8263Articles publicats en revistes (Bioquímica i Biomedicina Molecular)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésReproducció del document publicat a http://dx.doi.org/doi:10.1172/JCI116897Journal of Clinical Investigation, 1993, vol. 92, núm. 6, p. 2783-2789.(c) The American Society for Clinical Investigation, 1993info:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/82632026-05-27T06:46:51Z
dc.title.none.fl_str_mv Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model.
title Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model.
spellingShingle Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model.
Costelli, Paola
Tumors
Necrosi
Músculs
Tumor necrosis factor
Skeletal muscle
Protein turnover
title_short Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model.
title_full Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model.
title_fullStr Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model.
title_full_unstemmed Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model.
title_sort Tumor necrosis factor-alpha mediates changes in tissue protein turnover in a rat cancer cachexia model.
dc.creator.none.fl_str_mv Costelli, Paola
Carbó Carbó, Neus
Tessitore, Luciana
Bagby, Gregory J.
López-Soriano, Francisco J.
Argilés Huguet, Josep Ma.
Baccino, Francesco M.
author Costelli, Paola
author_facet Costelli, Paola
Carbó Carbó, Neus
Tessitore, Luciana
Bagby, Gregory J.
López-Soriano, Francisco J.
Argilés Huguet, Josep Ma.
Baccino, Francesco M.
author_role author
author2 Carbó Carbó, Neus
Tessitore, Luciana
Bagby, Gregory J.
López-Soriano, Francisco J.
Argilés Huguet, Josep Ma.
Baccino, Francesco M.
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Tumors
Necrosi
Músculs
Tumor necrosis factor
Skeletal muscle
Protein turnover
topic Tumors
Necrosi
Músculs
Tumor necrosis factor
Skeletal muscle
Protein turnover
description Rats bearing the Yoshida AH-130 ascites hepatoma showed enhanced fractional rates of protein degradation in gastrocnemius muscle, heart, and liver, while fractional synthesis rates were similar to those in non-tumor bearing rats. This hypercatabolic pattern was associated with marked perturbations of the hormonal homeostasis and presence of tumor necrosis factor in the circulation. The daily administration of a goat anti-murine TNF IgG to tumor-bearing rats decreased protein degradation rates in skeletal muscle, heart, and liver as compared with tumor-bearing rats receiving a nonimmune goat IgG. The anti-TNF treatment was also effective in attenuating early perturbations in insulin and corticosterone homeostasis. Although these results suggest that tumor necrosis factor plays a significant role in mediating the changes in protein turnover and hormone levels elicited by tumor growth, the inability of such treatment to prevent a reduction in body weight implies that other mediators or tumor-related events were also involved.
publishDate 1993
dc.date.none.fl_str_mv 1993
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/8263
url https://hdl.handle.net/2445/8263
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Reproducció del document publicat a http://dx.doi.org/doi:10.1172/JCI116897
Journal of Clinical Investigation, 1993, vol. 92, núm. 6, p. 2783-2789.
dc.rights.none.fl_str_mv (c) The American Society for Clinical Investigation, 1993
info:eu-repo/semantics/openAccess
rights_invalid_str_mv (c) The American Society for Clinical Investigation, 1993
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv American Society for Clinical Investigation
publisher.none.fl_str_mv American Society for Clinical Investigation
dc.source.none.fl_str_mv Articles publicats en revistes (Bioquímica i Biomedicina Molecular)
reponame:Dipòsit Digital de la UB
instname:Universidad de Barcelona
instname_str Universidad de Barcelona
reponame_str Dipòsit Digital de la UB
collection Dipòsit Digital de la UB
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,301629

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