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Liver protein synthesis and glycogen storage with the progression of cancer cachexia (649.2)

Cachexia is a multifactorial syndrome characterized by the loss of peripheral tissue and hypertrophy of visceral organs. The ApcMin/+ mouse model develops an IL‐6 dependent cachexia, leading to gradual loss of muscle and fat and hypertrophy of spleen and liver. The purpose of this study was to examine liver function related to protein synthesis and glycogen storage during the progression of cancer cachexia. Livers collected from non‐cachectic and cachectic ApcMin/+ mice were analyzed for marker of protein synthesis (p38) and degradation/angiogenesis marker ‐ MMP2 protein expression. Liver glycogen content was examined by PAS staining intensity. The role of cachexia related inflammation on liver metabolism was studied by 10mg/kg/day administration of PDTC, a STAT3 and NF‐ΚB inhibitor, for 2 weeks. As cachexia progressed there was suppression of Akt and p38 phosphorylation, and a reduction in liver glycogen content. MMP2 expression was also decreased 97% with severe cachexia. PDTC administration during severe cachexia did not rescue suppressed p38 phosphorylation or MMP2 expression. However, glycogen storage was increased in the PDTC treated cachectic Min mice as compared to the untreated mice. These results indicate that signaling regulating liver protein synthesis is suppressed with cachexia progression, and there is a loss of glycogen stores in severely cachectic mice, which is partially rescued by inhibition of STAT and NF‐ΚB signaling, irrespective of p38 suppression.