Degree
Master of Science
Program
Physiology
Supervisor
Dr. Nica Borradaile
Abstract
Obesity is associated with elevated levels of serum fatty acids, which accumulate in nonadipose tissues including the liver. Elongation factor 1A-1 (EF1A-1) has previously been shown to participate in the cell stress and death response of cardiomyocytes to excess saturated fatty exposure, and in steatotic mouse myocardium. In this thesis, the hypothesis that the hepatocyte response to fatty acid overload involves EF1A-1 was tested. EF1A-1 expression was induced in the livers of obese mice in association with severe hepatic steatosis, and in HepG2 human hepatoma cells in response to excess palmitate. Partial translocation of EF1A-1 from the ER to polymerized actin preceded palmitate-induced cell death. Inhibiting the elongation function of the protein using a specific inhibitor decreased palmitate-induced cell death. Results indicate EF1A-1 participates in hepatocyte stress response to saturated fatty acid excess possibly by mediating changes in protein synthesis related to actin cytoskeleton remodeling that occur during cell stress.
Recommended Citation
Stoianov, Alexandra M., "Elongation factor 1A-1 and hepatocyte response to fatty acid excess" (2013). Electronic Thesis and Dissertation Repository. 1210.
https://ir.lib.uwo.ca/etd/1210
Included in
Biochemistry Commons, Cellular and Molecular Physiology Commons, Nutritional and Metabolic Diseases Commons