Division of Nephrology and Hypertension, Department of Medicine, University of California-San Diego/Veterans Affairs San Diego Healthcare System, CA 92093-0711, USA.
J Am Soc Nephrol. 2010 Mar;21(3):406-12. doi: 10.1681/ASN.2009080820. Epub 2010 Feb 11.
Obesity is a risk factor for chronic kidney disease (CKD) and nonalcoholic fatty liver disease (NAFLD). Recent studies identify mechanisms common to both diseases linked through an interorgan communication orchestrated by fetuin-A and adiponectin. In liver and kidney, the energy sensor 5'-AMP activated protein kinase (AMPK) is pivotal to directing podocytes and hepatocytes to compensatory and potentially deleterious pathways, leading to inflammatory and profibrotic cascades culminating in end-organ damage. Regulation of these early upstream pathways may provide new therapeutic targets for these increasingly common sequelae of obesity.
肥胖是慢性肾脏病（CKD）和非酒精性脂肪肝疾病（NAFLD）的一个风险因素。最近的研究确定了两种疾病之间的共同机制，这些机制通过胎球蛋白-A 和脂联素协调的器官间通讯联系在一起。在肝脏和肾脏中，能量传感器 5'-AMP 激活蛋白激酶（AMPK）对于指导足细胞和肝细胞进入代偿性和潜在有害的途径至关重要，导致炎症和纤维形成级联反应，最终导致终末器官损伤。这些早期上游途径的调节可能为肥胖的这些越来越常见的后遗症提供新的治疗靶点。
