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Circulating IL‐6 and cancer cachexia in the Apc Min/+ mouse
Author(s) -
Baltgalvis Kristen A.,
Berger Franklin G.,
Pena Maria Marjorette O.,
Carson James A.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a943-c
Subject(s) - cachexia , medicine , gastrocnemius muscle , endocrinology , wasting , electroporation , muscle mass , chemistry , skeletal muscle , cancer , biochemistry , gene
Cachexia in Apc Min/+ 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 Apc Min/+ mouse. Apc Min/+ / 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 Apc Min/+ 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. Apc Min/+ / IL‐6 −/− mouse gastrocnemius muscle was resistant to wasting when compared to age‐matched Apc Min/+ mice (125 ± 5 mg vs. 93 ± 11 mg). IL‐6 overexpression did induce Apc Min/+ / 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 Apc Min/+ 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.