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. 2008 Feb;294(2):R393-401.
doi: 10.1152/ajpregu.00716.2007. Epub 2007 Dec 5.

Interleukin-6 and cachexia in ApcMin/+ mice

Kristen A Baltgalvis  1 , Franklin G Berger, Maria Marjorette O Pena, J Mark Davis, Stephanie J Muga, James A Carson
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Free article

Interleukin-6 and cachexia in ApcMin/+ mice

Kristen A Baltgalvis et al. Am J Physiol Regul Integr Comp Physiol. 2008 Feb.
Free article

Abstract

The Apc(Min/+) mouse has a mutation in the Apc tumor suppressor gene and develops intestinal polyps, beginning at 4 wk of age. This mouse develops cachexia by 6 mo, characterized by significant loss of muscle and fat tissue. The purpose of the present study was to determine the role of circulating interleukin-6 (IL-6) and the polyp burden for the development of cachexia in Apc(Min/+) mice. At 26 wk 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 with mildly cachectic animals. Apc(Min/+)/IL-6(-/-) mice did not lose gastrocnemius muscle mass or epididymal fat pad mass while overall polyp number decreased by 32% compared with Apc(Min/+) mice. Plasmid-based IL-6 overexpression in Apc(Min/+)/IL-6(-/-) mice led to a decrease in gastrocnemius muscle mass and epididymal fat pad mass and increased intestinal polyp burden. IL-6 overexpression 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 Apc(Min/+) mouse and that circulating IL-6 can regulate Apc(Min/+) mouse tumor burden.

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