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Am J Physiol Regul Integr Comp Physiol (December 5, 2007). doi:10.1152/ajpregu.00716.2007
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Submitted on October 4, 2007
Accepted on December 4, 2007

Interleukin-6 and Cachexia in ApcMin/+ Mice

Kristen A Baltgalvis1, Franklin G. Berger2, Maria Marjorette O Pena2, J. Mark Davis1, Stephanie J Muga3, and James A Carson1*

1 Exercise Science, University of South Carolina, Columbia, South Carolina, United States
2 Biological Sciences, University of South Carolina, Columbia, South Carolina, United States
3 Cellular and Molecular Pharmacology, Medical University of South Carolina, Charleston, South Carolina, United States

* To whom correspondence should be addressed. E-mail: carsonj{at}gwm.sc.edu.

The ApcMin/+ mouse has a mutation in the Apc tumor suppressor gene and develops intestinal polyps, beginning at 4 weeks of age. This mouse develops cachexia by 6 months, characterized by significant loss of muscle and fat tissue. The purpose of the present study was to determine the role of circulating IL-6 and the polyp burden for the development of cachexia in ApcMin/+ mice. At 26 weeks of age, mice exhibiting severe cachectic symptoms had a 61% decrease in gastrocnemius muscle weight, complete loss of epididymal fat, a 10-fold increase in circulating IL-6 levels, and an 89% increase in intestinal polyps compared to mildly cachectic animals. ApcMin/+ / IL-6-/- mice did not lose gastrocnemius muscle mass or epididymal fat pad mass, while overall polyp number decreased by 32% compared to ApcMin/+ mice. Plasmid-based IL-6 over-expression in ApcMin/+ / IL-6-/- mice led to a decrease in gastrocnemius muscle mass, epididymal fat pad mass, and increased intestinal polyp burden. IL-6 over-expression did not induce cachexia in non-tumor bearing mice. These data demonstrate that IL-6 is necessary for the onset of adipose and skeletal muscle wasting in the ApcMin/+ mouse and that circulating IL-6 can regulate ApcMin/+ mouse tumor burden.




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