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Full-Text Articles in Physiology
Pathogenesis And Therapeutic Considerations For Nonalcoholic Fatty Liver Disease, Elijah Chung
Pathogenesis And Therapeutic Considerations For Nonalcoholic Fatty Liver Disease, Elijah Chung
Senior Honors Theses
A product of the Westernized, high-fat diet, non-alcoholic fatty liver disease (NAFLD) has emerged as the leading cause of chronic liver disease, affecting one-fourth of the world's population. NAFLD is a progressive disease arising from a multisystem response to excess lipids in the blood, adipose tissue, and liver. Despite the prevalence of NAFLD and its well-studied bidirectional association with obesity and type 2 diabetes mellitus and obesity, there is a shocking scarcity of available treatments aside from diet and lifestyle changes. Thus, further research on NAFLD and potential therapies is urgently needed. This paper will illustrate the major pathways associated …
Maintenance Of Mitochondrial Genomic Integrity In The Absence Of Manganese Superoxide Dismutase In Mouse Liver Hepatocytes., Anthony R. Cyr, Kyle E. Brown, Michael L. Mccormick, Mitchell C. Coleman, Adam J. Case, George S. Watts, Bernard W. Futscher, Douglas R. Spitz, Frederick E. Domann
Maintenance Of Mitochondrial Genomic Integrity In The Absence Of Manganese Superoxide Dismutase In Mouse Liver Hepatocytes., Anthony R. Cyr, Kyle E. Brown, Michael L. Mccormick, Mitchell C. Coleman, Adam J. Case, George S. Watts, Bernard W. Futscher, Douglas R. Spitz, Frederick E. Domann
Journal Articles: Cellular & Integrative Physiology
Manganese superoxide dismutase, encoded by the Sod2 gene, is a ubiquitously expressed mitochondrial antioxidant enzyme that is essential for mammalian life. Mice born with constitutive genetic knockout of Sod2 do not survive the neonatal stage, which renders the longitudinal study of the biochemical and metabolic effects of Sod2 loss difficult. However, multiple studies have demonstrated that tissue-specific knockout of Sod2 in murine liver yields no observable gross pathology or injury to the mouse. We hypothesized that Sod2 loss may have sub-pathologic effects on liver biology, including the acquisition of reactive oxygen species-mediated mitochondrial DNA mutations. To evaluate this, we established …