| Theme | NASH : An Update | |
|---|---|---|
| Title | NASH and Metabolic Syndrome | |
| Publish Date | 2007/10 | |
| Author | Kenichi Ikejima | Department of Gastroenterology, Juntendo University School of Medicine |
| Author | Kazuyoshi Kon | Department of Gastroenterology, Juntendo University School of Medicine |
| Author | Tomonori Aoyama | Department of Gastroenterology, Juntendo University School of Medicine |
| Author | Shunhei Yamashina | Department of Gastroenterology, Juntendo University School of Medicine |
| Author | Satoko Suzuki | Department of Gastroenterology, Juntendo University School of Medicine |
| Author | Sumio Watanabe | Department of Gastroenterology, Juntendo University School of Medicine |
| [ Summary ] | Nonalcoholic fatty liver disease (NAFLD) is a common feature of metabolic syndrome, which is associated with obesity, type 2 diabetes, hyperlipidemia and hypertension. The disease spectrum of NAFLD ranges from simple steatosis to nonalcoholic steatohepatitis (NASH) exhibiting a wide range of inflammatory degree and fibrosis stages. The complex interaction of genetics, environmental factors and nutritional / lifestyle conditions remains to be well elucidated. However, insulin resistance is believed to be crucial in the pathogenesis of steatohepatitis. Inflammatory mediators including tumor necrosis factor (TNF) - α and intracellular signaling molecules such as peroxisome proliferator-activated receptors (PPAR) coordinately regulate insulin sensitivity, suggesting that insulin resistance and hepatic inflammation aggravate each other. Both humoral and nervous regulators also play important roles in the progression of NASH. It is notable that the expression profiles of adipokines modulate metabolic, inflammatory and profibrogenic responses in the liver. Furthermore, the rennin-angiotensin system and the autonomic nervous system are not only important in the control of blood pressure but also in the progression of steatohepatitis. Therefore, it is postulated that molecular targeting of these pathways enables comprehensive therapeutics for metabolic syndrome-related atherosclerotic diseases and steatoheptitis. | |