Center for Liver Disease and Transplantation, New York Presbyterian Hospital, Columbia University College of Physicians and Surgeons, New York, USA.
Adv Ther. 2009 Oct;26(10):893-907. doi: 10.1007/s12325-009-0072-z. Epub 2009 Nov 16.
Nonalcoholic fatty liver disease (NAFLD), first described in 1980, is now recognized as one of the most common causes of elevated liver enzymes and chronic liver disease in Western countries. The incidence of NAFLD in both adults and children is rising, in conjunction with the burgeoning epidemics of obesity and type 2 diabetes mellitus. NAFLD often coexists with other sequelae of the metabolic syndrome: central obesity, type 2 diabetes, hypertension, and hyperlipidemia. NAFLD encompasses a spectrum of pathologic liver diseases ranging from simple hepatic steatosis to a predominant lobular necro-inflammation, with or without centrilobular fibrosis (called nonalcoholic steatohepatitis or NASH). NASH can progress to cirrhosis, decompensated liver disease, and hepatocellular carcinoma. Though the natural history of NASH is still not clearly defined, it has been observed to progress to cirrhosis in 15%-220% of those affected. Insulin resistance is nearly universal in NASH and is thought to play an important role in its pathogenesis leading to dysregulated lipid metabolism. The prevalence of insulin resistance is reported in the general population to be approaching 45%, suggesting that NAFLD and NASH will contin nue to be an important public health concern. To date, NASH has proven to be a difficult disease to treat. Front-line therapy with lifestyle modifications resulting in weight loss through decreased caloric intake and moderate exercise is generally believed to be beneficial in patients with NASH, but is often difficult to maintain long term. Given that insulin resistance plays a dominant role in the pathogenesis, many studies have examined the use of insulin sensitizers: the biguanides (metformin), thiazolidinediones (pioglitazone, troglitazone, and rosiglitazone), glucagon-like peptide-1-receptor agonists, or incretins (exenatide)in NASH. This review will provide an overview of insulin resistance in NAFLD and provide a detailed summary on the clinical data regarding the use of insulin sensitizers in NASH.
非酒精性脂肪性肝病(NAFLD)于 1980 年首次描述,现已被认为是西方国家引起肝酶升高和慢性肝病的最常见原因之一。NAFLD 在成人和儿童中的发病率都在上升,同时肥胖症和 2 型糖尿病的流行也在增加。NAFLD 常与代谢综合征的其他后遗症并存:中心性肥胖、2 型糖尿病、高血压和高脂血症。NAFLD 包含一系列从单纯肝脂肪变性到以小叶坏死性炎症为主、伴有或不伴有中央纤维化为特征的肝脏疾病(称为非酒精性脂肪性肝炎或 NASH)。NASH 可进展为肝硬化、失代偿性肝病和肝细胞癌。虽然 NASH 的自然史尚不清楚,但据观察,在 15%-220%的患者中可进展为肝硬化。胰岛素抵抗在 NASH 中几乎普遍存在,被认为在其发病机制中发挥重要作用,导致脂质代谢失调。据报道,普通人群中胰岛素抵抗的患病率接近 45%,这表明 NAFLD 和 NASH 将继续成为一个重要的公共卫生问题。迄今为止,NASH 的治疗已被证明是一项困难的工作。一线治疗方法是通过减少热量摄入和适度运动来减轻体重,从而改变生活方式,一般认为对 NASH 患者有益,但往往难以长期维持。鉴于胰岛素抵抗在发病机制中起主导作用,许多研究都研究了胰岛素增敏剂的使用:双胍类(二甲双胍)、噻唑烷二酮类(吡格列酮、罗格列酮和曲格列酮)、胰高血糖素样肽-1 受体激动剂或肠促胰岛素(艾塞那肽)在 NASH 中的应用。这篇综述将概述 NAFLD 中的胰岛素抵抗,并详细总结胰岛素增敏剂在 NASH 中的临床数据。