Date of Graduation


Document Type


Degree Name

Bachelor of Science Education

Degree Level



Health, Human Performance and Recreation


Greene, Nicholas

Committee Member/Reader

Washington, Tyrone

Committee Member/Second Reader

Howie, Erin

Committee Member/Third Reader


Committee Member/Fourth Reader



BACKGROUND: Cancer cachexia is defined as cancer-associated muscle wasting, and is a cancer side effect that dramatically affects cancer prognosis, is thought to be at least partially mediated by increased energy expenditure, and is directly responsible for the death of 20-40% of all cancer patients. Although the liver is known to be a predominant regulator of whole body metabolism, there is little known about its relationship to the development of cancer cachexia. PURPOSE: The purpose of this exploratory study was to investigate alterations in liver metabolism by examining measures of hepatic glycogen storage, oxidative phenotype and lipid content throughout the progression of Lewis Lung Carcinoma (LLC)-induced cancer cachexia. METHODS: C57BL/6J mice were injected with 1X106 LLC cells in the hind flank, and the control group with phosphate buffered saline (PBS). The experimental groups included PBS, 1wk, 2wk, 3wk, and 4wk of cancer progression with 10-16 in each group. Sections of liver (n=~8/group) were cut and stains for hepatic glycogen content (Periodic Acid Schiff), lipid content (Oil Red O) and oxidative phenotype (SDH) were completed. Images were acquired using Nikon TiS epifluorescent microscope and analyzed using NIS-Elements imaging software. A one-way analysis of variance was used to determine differences between groups, where significant F ratios were found a Tukey post hoc was used to determine differences between means. Significance was denoted at p0.05) or SDH percent area (p>0.05) and intensity of stain (p>0.05). PAS percent area of stain was different at 3 wks compared to 1 and 2 wks (p= 0.0094), but there were no differences detected in intensity of PAS stain (p>0.05). CONCLUSION: Differences in liver sizes do not appear to be attributable to glycogen storage, oxidative phenotype or lipid content. Though there were no differences found, the increase in liver size suggests disruption of other processes in the liver. For future projects, we will further investigate mechanisms of hepatic hypertrophy in order to determine the relationship between the liver and cancer cachexia progression.


hepatic phenotype, cancer cachexia, oxygen content, progression, liver, glycogen