Abstract
Obesity with associated comorbidities is currently a worldwide epidemic and among the most challenging health conditions in the 21st century. A major metabolic consequence of obesity is insulin resistance which underlies the pathogenesis of the metabolic syndrome. Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of obesity and metabolic syndrome. It comprises a disease spectrum ranging from simple steatosis (fatty liver), through nonalcoholic steatohepatitis (NASH) to fibrosis, and ultimately liver cirrhosis. Abnormality in lipid and lipoprotein metabolism accompanied by chronic inflammation is the central pathway for the development of metabolic syndrome-related diseases, such as atherosclerosis, cardiovascular disease (CVD), and NAFLD. This paper focuses on pathogenic aspect of lipid and lipoprotein metabolism in NAFLD and the relevant mouse models of this complex multifactorial disease.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is progressively diagnosed worldwide and is considered to be the most common liver disorder in Western countries, estimated to affect at least one-quarter of the general population [1, 2]
Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of obesity and metabolic syndrome. It comprises a disease spectrum ranging from simple steatosis, through nonalcoholic steatohepatitis (NASH) to fibrosis, and liver cirrhosis
This paper focuses on pathogenic aspect of lipid and lipoprotein metabolism in NAFLD and the relevant mouse models of this complex multifactorial disease
Summary
Nonalcoholic fatty liver disease (NAFLD) is progressively diagnosed worldwide and is considered to be the most common liver disorder in Western countries, estimated to affect at least one-quarter of the general population [1, 2]. NAFLD covers a spectrum of hepatic pathologies, ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) It strongly associates with obesity, insulin resistance, hypertension, and dyslipidaemia and is regarded as the liver manifestation of metabolic syndrome [6]. Abnormalities in lipid and lipoprotein metabolism accompanied by chronic inflammation are considered to be the central pathway for the development of several obesity-related co-morbidities such as NAFLD and cardio-vascular disease (CVD) [8, 9]. In NAFLD patients, liver overproduces several atherogenic factors, such as cytokines and “bad” lipoproteins In this manner, fatty liver is associated with increased serum low-density lipoproteins (LDL) and triglycerides, combined with decreased highdensity lipoproteins (HDL) that represent a threat for CVD development (reviewed in [10]). We briefly discuss how reviewed pathways are involved in the therapeutic strategies for NAFLD
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