In 1980, Ludwig et al. first reported patients of steatohepatitis who lacked a history of excessive alcohol consumption but showed liver histology resembling alcoholic hepatitis and progression to cirrhosis of the liver accompanied by inflammation and fibrosis. The development of nonalcoholic steatohepatitis (NASH) is associated with obesity, diabetes mellitus, insulin resistance, and hyperlipidemia. However, the pathogenesis of NASH remains incomplete. A "multiple-hit" hypothesis for the pathogenesis of NASH based on an animal model has been proposed and remains a foundation for research in this field. We review the important dietary and genetic animal models and discuss the pathogenesis of NASH.
Keyphrases
- insulin resistance
- alcohol consumption
- end stage renal disease
- metabolic syndrome
- high fat diet induced
- high fat diet
- type diabetes
- chronic kidney disease
- newly diagnosed
- ejection fraction
- liver fibrosis
- oxidative stress
- weight gain
- adipose tissue
- weight loss
- skeletal muscle
- prognostic factors
- polycystic ovary syndrome
- peritoneal dialysis
- liver injury
- genome wide
- gene expression
- copy number
- dna methylation
- drug induced