Pathogenesis of nonalcoholic steatohohepatitis [sic] : the role of CYP2E1
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Open Access
Type
ThesisThesis type
Doctor of PhilosophyAuthor/s
Weltman, Martin D. (Martin David)Abstract
The relevant literature concerning nonalcoholic steatohepatitis (NASH), the
morphologically similar condition of alcoholic liver disease (ALD), and the hepatic
cytochromes P450 (P450 or CYP) was reviewed with particular emphasis on
CYP2E1. CYP2E1 is induced in ALD. It plays an ...
See moreThe relevant literature concerning nonalcoholic steatohepatitis (NASH), the morphologically similar condition of alcoholic liver disease (ALD), and the hepatic cytochromes P450 (P450 or CYP) was reviewed with particular emphasis on CYP2E1. CYP2E1 is induced in ALD. It plays an important role in the pathogenesis of this condition by generating reactive oxygen species (ROS). In turn, ROS produce lipid peroxidation, which contributes to the cellular injury in ALD. CYP2E1 is constitutively expressed in acinar zone 3. The early lesions observed in both ALD and NASH are most pronounced in the same acinar region of the liver. Since NASH and ALD have similar histological appearances, the possibility that CYP2E1 may play a significant role in the pathogenesis of NASH was considered. One of the limitations in evaluating the pathogenesis of NASH has been the absence of an appropriate animal model.
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See moreThe relevant literature concerning nonalcoholic steatohepatitis (NASH), the morphologically similar condition of alcoholic liver disease (ALD), and the hepatic cytochromes P450 (P450 or CYP) was reviewed with particular emphasis on CYP2E1. CYP2E1 is induced in ALD. It plays an important role in the pathogenesis of this condition by generating reactive oxygen species (ROS). In turn, ROS produce lipid peroxidation, which contributes to the cellular injury in ALD. CYP2E1 is constitutively expressed in acinar zone 3. The early lesions observed in both ALD and NASH are most pronounced in the same acinar region of the liver. Since NASH and ALD have similar histological appearances, the possibility that CYP2E1 may play a significant role in the pathogenesis of NASH was considered. One of the limitations in evaluating the pathogenesis of NASH has been the absence of an appropriate animal model.
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Date
1998Rights statement
The author retains copyright of this thesis. It may only be used for the purposes of research and study. It must not be used for any other purposes and may not be transmitted or shared with others without prior permission.Faculty/School
Faculty of MedicineDepartment, Discipline or Centre
Department of MedicineAwarding institution
The University of SydneyShare