Blood glucose levels were also lower between Rad and KC+Rad on day 6 but not on day 13. Our results did not demonstrate a correlation between circulating glucose levels and survival, suggesting that the anti-tumor effects seen are likely to be due to more than just reduced glucose levels. In addition, we did not find a change in body D-Pantothenic acid sodium weight between animals fed KC ad Hexyl Chloroformate libitum and animals fed SD ad libitum. A drop in weight was seen in animals treated with KC in combination with radiation around day 6; however, animals regained this weight by day 15. No direct relationship was seen between weight loss and ketone or blood glucose levels or between blood glucose levels and survival. The KC and KC plus radiation cohort showed the longest survival without a statistical difference in either blood glucose or weight loss. This agrees with the results of our earlier work and serves to further the notion that survival may be independent of blood glucose levels. In our previous work we used a syngeneic bioluminescent intracranial tumor model to show that a,6:1 rodent KD caused a 6 day increase in median survival of animals given unrestricted amounts of the KD, despite the fact that there was no measureable decrease in blood glucose. Furthermore, the dynamics of tumor growth demonstrated by in vivo imaging of implanted GL261-luc cells demonstrated a reduction in the rate of tumor growth in animals fed KD, just as we now report using KC. Molecular analyses of tumor and non-tumor tissue showed a reduction in reactive oxygen species in the tumor from animals fed the KD. A reduction in ROS was also shown in cultured GL261 cells when ketone bodies were added to complete media in vitro, providing additional evidence for some efficacy even in the absence of reduced glucose. Seyfried et al suggested that radiation and chemotherapy may promote a more favorable metabolic environment for glioma growth, thus reducing long term survival. While there may be local increases in blood glucose and/or glutamine in our model system, we did not see an increase in blood glucose in the animals treated with radiation. Furthermore, we did see a highly significant increase in long term survival. The profound survival increase seen in animals treated with KC and radiation may be due to the increased radiation cytotoxicity of tumor cells as a result of sensitization by KC due to the systemic effects of this diet. Similar results have been reported in the literature. The regulation of glucose in cells treated with cisplatin and carboplatin enhanced their sensitivity. Cells cultured with 2-deoxyglucose had a 1.8 to 2.6 fold increase in cellular sensitivity to cisplatin.