colon 26 adenocarcinoma (c26)-induced cancer cachexia impairs skeletal muscle mitochondrial function and content

The present study aimed to determine the impact of colon 26 adenocarcinoma (c26)-induced cancer cachexia on skeletal muscle mitochondrial respiration and content. twelve male cd2f1 mice were injected with c26-cells (tumor bearing (tb) group), whereas 12 age-matched mice received pbs vehicle injection (non-tumor bearing (n-tb) group). mitochondrial respiration was studied in saponin-permeabilized soleus myofibers. tb mice showed lower body weight (~ 20%) as well as lower soleus, gastrocnemius-plantaris complex and tibialis anterior masses versus n-tb mice (p < 0.05). soleus maximal state iii mitochondrial respiration was 20% lower (10 mm glutamate, 5 mm malate, 5 mm adenosine diphosphate; p < 0.05) and acceptor control ratio (state iii/state ii) was 15% lower in the tb vs. n-tb (p < 0.05), with the latter suggesting uncoupling. lower vdac protein content suggested reduced mitochondrial content in tb versus n-tb (p < 0.05). skeletal muscle in c26-induced cancer cachexia exhibits reductions in: maximal mitochondrial respiration capacity, mitochondrial coupling and mitochondrial content.