Definition, Pathogenesis, and Natural Progress of Non-alcoholic Fatty Liver Disease.
- Author:
Jae Han JEON
1
;
Keun Gyu PARK
Author Information
- Publication Type:Original Article
- Keywords: Free fatty acid; Insulin resistance; Non-alcoholic fatty liver disease; Obesity
- MeSH: Adipose Tissue; Ceramides; Diglycerides; Endoplasmic Reticulum Stress; Fatty Liver*; Fibrosis; Glucose; Hepatic Stellate Cells; Inflammation; Insulin Resistance; Lipogenesis; Lipolysis; Liver; Liver Cirrhosis; Lysophosphatidylcholines; Muscle, Skeletal; Obesity
- From:Journal of Korean Diabetes 2014;15(2):65-70
- CountryRepublic of Korea
- Language:Korean
- Abstract: Non-alcoholic fatty liver disease (NAFLD) is emerging as a world-wide health problem and is currently recognized as a hepatic manifestation of metabolic syndrome. It is an umbrella term to describe a wide range of diseases from simple steatosis to non-alcoholic hepatosteatosis (NASH) and NSAH-related liver cirrhosis. NAFLD is mainly associated with insulin resistance which allows increased free fatty acid (FFA) flux to the liver by increasing lipolysis from adipose tissue, triggering macrophage/immune activation, decreasing skeletal muscle glucose uptake, and increasing de novo lipogenesis. Increased FFA pool in the liver, in turn, increases lipotoxic intermediates, such as ceramides, diacylglycerols, and lysophosphatidylcholines, which are responsible for mitochondrial dysfunction and endoplasmic reticulum stress, resulting in inflammation of the liver. When inflammation is severe enough to affect stellate cells, hepatic fibrosis can be induced.
