| Theme | NASH : An Update | |
|---|---|---|
| Title | NASH and Hepatocarcinogenesis | |
| Publish Date | 2007/10 | |
| Author | Kyoji Moriya | Department of Infection Control and Prevention, The University of Tokyo Hospital |
| Author | Hideyuki Miyoshi | Department of Gastroenterology, The University of Tokyo Hospital |
| Author | Kazuhiko Koike | Department of Infection Diseases, The University of Tokyo Hospital |
| [ Summary ] | Hepatic steatosis is a prerequisite for many subsequent events that lead to liver injury. Several lines of evidence suggest that mitochondrial function is impaired in patients with NASH and HCV. Impaired mitochondria activity leads to the formation of ROS and steatosis. ROS and products of lipid peroxidation can lead to fibrosis. A steatotic liver may further contribute to the development of insulin resistance. Hepatic steatosis, insulin resistance, and type II diabetes have been observed to occur more frequently in association with HCV infection and NASH than other chronic inflammatory liver diseases. Dysfunctions related to energetic homeostasis and the interaction of adiponectin, leptin and tumour necrosis factor-alpha are key events in the pathogenesis of steatosis and insulin resistance. Insulin resistance is emerging as a major risk factor for a wide variety of cancers, including hepatocellular carcinoma. Insulin resistance is associated with increased risk of hepatic cancer. | |