Abstract
Cachexia in ApcMin/+ mice is associated with chronic elevation of plasma IL-6. The purpose of this study was to examine the ability of IL-6 to induce cachexia in the ApcMin/+ mouse. ApcMin/+ / IL-6−/− mice were used to study the effect of IL-6 depletion. Electroporation of an IL-6 expression plasmid into the mouse quadriceps muscle was used to chronically increase circulating IL-6, while the empty vector served as the control. Four weeks of electroporation in ApcMin/+ mice increased circulating IL-6 levels from 9.7 ± 2.8 pg/ml to 181.1 ± 29.6 pg/ml, and accelerated gastrocnemius muscle mass loss 23% (115 ± 10 vs. 88 ± 5 mg). The rate of epididymal fat pad mass loss was also accelerated by 70% (165 ± 52 vs. 49 ± 13 mg) compared to controls. ApcMin/+ / IL-6−/− mouse gastrocnemius muscle was resistant to wasting when compared to age-matched ApcMin/+ mice (125 ± 5 mg vs. 93 ± 11 mg). IL-6 overexpression did induce ApcMin/+ / IL-6−/− mice gastrocnemius muscle wasting (121 ± 11 vs. 71 ± 8 mg) and epididymal fat pad mass loss (209 ± 50 vs. 3 ± 3 mg) compared to empty vector controls. Increased circulating IL-6 is sufficient to accelerate ApcMin/+ mouse cachexia and this effect is independent of tissue level IL-6 expression. This research was supported by National Center for Research Resources Grant P20 RR-017698.
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