Fon Tacer Klementina, Rozman Damjana
Center for Functional Genomic and Biochips, Institute of Biochemistry, Faculty of Medicine, University of Ljubljana, Zaloška 4, 1000 Ljubljana, Slovenia.
J Lipids. 2011;2011:783976. doi: 10.1155/2011/783976. Epub 2011 Jul 2.
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.
肥胖及其相关合并症目前是一种全球性流行病，也是21世纪最具挑战性的健康问题之一。肥胖的一个主要代谢后果是胰岛素抵抗，它是代谢综合征发病机制的基础。非酒精性脂肪性肝病（NAFLD）是肥胖和代谢综合征的肝脏表现。它包括一个疾病谱，从单纯性脂肪变性（脂肪肝），到非酒精性脂肪性肝炎（NASH），再到纤维化，最终发展为肝硬化。脂质和脂蛋白代谢异常伴有慢性炎症是代谢综合征相关疾病（如动脉粥样硬化、心血管疾病（CVD）和NAFLD）发展的核心途径。本文重点关注NAFLD中脂质和脂蛋白代谢的致病方面以及这种复杂多因素疾病的相关小鼠模型。
