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Induction of muscle protein degradation by a tumour factor

Induction of muscle protein degradation by a tumour factor An antigen of apparent molecular weight of 24,000, reactive with a murine monoclonal antibody, has been isolated from a cachexia-inducing tumour (MAC 16) and has been shown to initiate muscle protein degradation in vitro using isolated soleus muscle. Administration of this material to female NMRI mice (20 g) produced a pronounced depression in body weight (2.72 +/- 0.14 g; P<0.005 from control) over a 24 h period. This weight loss was attenuated in mice pretreated with the monoclonal antibody (0.06 +/- 0.26 g over 24 h) and occurred without a reduction in food and water intake. There was no change in body water composition, and the major contribution to the decrease in body weight was a decrease in the non-fat carcass dry weight (mainly lean body mass). The plasma levels of glucose and most amino acids were also significantly depressed. The decrease in lean body mass was accounted for by an increase (by 50%) in protein degradation and a decrease (by 50%) in protein synthesis in gastrocnemius muscle. Protein degradation was significantly decreased and protein synthesis increased to control values in mice pretreated with the monoclonal antibody. Protein degradation initiated in vitro with the proteolysis-inducing factor was abolished in mice pretreated with eicosapentaenoic acid (EPA), which had been shown to prevent muscle wastage in mice bearing the MAC16 tumour. Protein degradation was associated with a significant elevation of prostaglandin E2 production by isolated soleus muscle, which was inhibited by both the monoclonal antibody and EPA. These results suggest that this material may be the humoral factor mediating changes in skeletal muscle protein homeostasis during the process of cancer cachexia in animals bearing the MAC16 tumour, and could potentially be involved in other cases of cachexia. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png British Journal of Cancer Springer Journals

Induction of muscle protein degradation by a tumour factor

Lorite, MJ; Cariuk, P; Tisdale, MJ
British Journal of Cancer , Volume 76 (8) – Oct 1, 1997
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References (34)

Publisher
Springer Journals
Copyright
Copyright © 1997 by Cancer Research Campaign
Subject
Biomedicine; Biomedicine, general; Cancer Research; Epidemiology; Molecular Medicine; Oncology; Drug Resistance
ISSN
0007-0920
eISSN
1532-1827
DOI
10.1038/bjc.1997.504
Publisher site
See Article on Publisher Site

Abstract

An antigen of apparent molecular weight of 24,000, reactive with a murine monoclonal antibody, has been isolated from a cachexia-inducing tumour (MAC 16) and has been shown to initiate muscle protein degradation in vitro using isolated soleus muscle. Administration of this material to female NMRI mice (20 g) produced a pronounced depression in body weight (2.72 +/- 0.14 g; P<0.005 from control) over a 24 h period. This weight loss was attenuated in mice pretreated with the monoclonal antibody (0.06 +/- 0.26 g over 24 h) and occurred without a reduction in food and water intake. There was no change in body water composition, and the major contribution to the decrease in body weight was a decrease in the non-fat carcass dry weight (mainly lean body mass). The plasma levels of glucose and most amino acids were also significantly depressed. The decrease in lean body mass was accounted for by an increase (by 50%) in protein degradation and a decrease (by 50%) in protein synthesis in gastrocnemius muscle. Protein degradation was significantly decreased and protein synthesis increased to control values in mice pretreated with the monoclonal antibody. Protein degradation initiated in vitro with the proteolysis-inducing factor was abolished in mice pretreated with eicosapentaenoic acid (EPA), which had been shown to prevent muscle wastage in mice bearing the MAC16 tumour. Protein degradation was associated with a significant elevation of prostaglandin E2 production by isolated soleus muscle, which was inhibited by both the monoclonal antibody and EPA. These results suggest that this material may be the humoral factor mediating changes in skeletal muscle protein homeostasis during the process of cancer cachexia in animals bearing the MAC16 tumour, and could potentially be involved in other cases of cachexia.

Journal

British Journal of Cancer – Springer Journals

Published: Oct 1, 1997

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