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Research Article Free access | 10.1172/JCI117276

Systemic administration of ciliary neurotrophic factor induces cachexia in rodents.

J T Henderson, N A Seniuk, P M Richardson, J Gauldie, and J C Roder

Samuel Lunenfeld Research Institute, Division of Neurobiology and Molecular Immunology, Mount Sinai Hospital, Toronto, Ontario, Canada.

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Samuel Lunenfeld Research Institute, Division of Neurobiology and Molecular Immunology, Mount Sinai Hospital, Toronto, Ontario, Canada.

Find articles by Seniuk, N. in: PubMed | Google Scholar

Samuel Lunenfeld Research Institute, Division of Neurobiology and Molecular Immunology, Mount Sinai Hospital, Toronto, Ontario, Canada.

Find articles by Richardson, P. in: PubMed | Google Scholar

Samuel Lunenfeld Research Institute, Division of Neurobiology and Molecular Immunology, Mount Sinai Hospital, Toronto, Ontario, Canada.

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Samuel Lunenfeld Research Institute, Division of Neurobiology and Molecular Immunology, Mount Sinai Hospital, Toronto, Ontario, Canada.

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Published June 1, 1994 - More info

Published in Volume 93, Issue 6 on June 1, 1994
J Clin Invest. 1994;93(6):2632–2638. https://doi.org/10.1172/JCI117276.
© 1994 The American Society for Clinical Investigation
Published June 1, 1994 - Version history
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Abstract

Ciliary neurotrophic factor (CNTF) has previously been shown to promote the survival of several classes of neurons and glial. We report here that in addition to its effects on the nervous system, CNTF can induce potent effects in extra-neural tissues. Implantation of C6 glioma cells engineered to secrete CNTF either subcutaneously or into the peritoneal cavity of adult mice, or systemic injections of purified rat or human recombinant CNTF, resulted in a rapid syndrome of weight loss resulting in death over a period of 7-10 d. This weight loss could not be explained by a reduction in food intake and involved losses of both fat and skeletal muscle. CNTF also induced the synthesis of acute phase proteins such as haptoglobin. Implantation of C6 lines expressing a nonsecreted form of CNTF, or the parental C6 line itself, did not result in wasting effects. Analysis of this CNTF-induced wasting indicates similarities with the previously described cachectins, tumor necrosis factor, interleukin 6, and leukemia inhibitory factor, but does not involve the induction of these cytokines.

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