Hepatocellular endothelial nitric oxide synthase and mitochondrial function in nonalcoholic steatohepatitis
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[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Nonalcoholic steatohepatitis (NASH) is the most rapidly growing liver disease in the United States. The development of treatments for this disease has been limited by a lack of understanding of the underlying cause(s). This dissertation identifies impaired activity of the enzyme called endothelial nitric oxide synthase (eNOS) as a novel cause of NASH. Specifically, mice that lack eNOS have increased susceptibility to NASH when fed a high-fat, western style diet. The data indicate that eNOS regulates the quality of liver mitochondria, which produce the energy necessary for normal liver function. Future work to manipulate eNOS function towards the treatment of NASH is necessary.
At author's request, access is limited to the campuses of the University of Missouri.