Department of Metabolic Medicine/Chemical Pathologyemical Pathology, Guy's and St. Thomas' Hospitals, London, UK.
Curr Opin Lipidol. 2012 Aug;23(4):345-52. doi: 10.1097/MOL.0b013e3283541cfc.
This article reviews the mechanisms leading to the development of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) and the effects of hypoglycaemic and lipid-lowering therapies on NAFLD/NASH.
The interaction of lipogenesis, fatty acid oxidation, inflammation, endoplasmic reticulum stress and hepatic insulin resistance contribute to the pathogenesis of NAFLD/NASH. Few large scale clinical trials exist with biopsy or magnetic resonance endpoints as opposed to ultrasonographic and transaminase endpoints. Trial evidence that exists supports the utility of weight loss, metformin, thiazolidinediones, fibrates, niacin, ezetimibe and statins in improving the steatosis component of NAFLD/NASH though with less or minimal effects on the fibrotic component of NASH.
Hypoglycaemic and lipid-lowering therapies may have a role in the treatment of NAFLD/NASH but large scale endpoint trials remain to be performed.
本文综述了导致非酒精性脂肪性肝病（NAFLD）和非酒精性脂肪性肝炎（NASH）发生的机制，以及降糖和调脂治疗对 NAFLD/NASH 的影响。
脂肪生成、脂肪酸氧化、炎症、内质网应激和肝胰岛素抵抗的相互作用导致了 NAFLD/NASH 的发病机制。与超声和转氨酶终点相比，很少有大型临床试验具有活检或磁共振终点。现有的试验证据支持减肥、二甲双胍、噻唑烷二酮类、贝特类、烟酸、依折麦布和他汀类药物在改善 NAFLD/NASH 的脂肪变性成分方面的作用，但对 NASH 的纤维化成分的影响较小或几乎没有。
降糖和调脂治疗可能在 NAFLD/NASH 的治疗中有一定作用，但仍需要进行大规模的终点试验。
