Department of Food Science and Human Nutrition, Colorado State University, Fort Collins, CO 80523, USA.
Biofactors. 2011 Jan-Feb;37(1):8-16. doi: 10.1002/biof.135. Epub 2010 Dec 2.
Nonalcoholic fatty liver disease (NAFLD) represents a burgeoning public health concern in westernized nations. The obesity-related disorder is associated with an increased risk of cardiovascular disease, type 2 diabetes and liver failure. Although the underlying pathogenesis of NAFLD is unclear, increasing evidence suggests that excess saturated fatty acids presented to or stored within the liver may play a role in both the development and progression of the disorder. A putative mechanism linking saturated fatty acids to NAFLD may be endoplasmic reticulum (ER) stress. Specifically, excess saturated fatty acids may induce an ER stress response that, if left unabated, can activate stress signaling pathways, cause hepatocyte cell death, and eventually lead to liver dysfunction. In the current review we discuss the involvement of saturated fatty acids in the pathogenesis of NAFLD with particular emphasis on the role of ER stress.
非酒精性脂肪性肝病(NAFLD)是西方工业化国家日益引人关注的公共健康问题。这种与肥胖相关的疾病与心血管疾病、2 型糖尿病和肝衰竭的风险增加有关。尽管 NAFLD 的潜在发病机制尚不清楚,但越来越多的证据表明,肝脏中存在或储存的过量饱和脂肪酸可能在该疾病的发生和发展中起作用。将饱和脂肪酸与 NAFLD 联系起来的一个假设机制可能是内质网(ER)应激。具体来说,过量的饱和脂肪酸可能会诱导内质网应激反应,如果不加控制,内质网应激反应可能会激活应激信号通路,导致肝细胞死亡,并最终导致肝功能障碍。在本综述中,我们讨论了饱和脂肪酸在 NAFLD 发病机制中的作用,特别强调了内质网应激的作用。