Obesity is a risk factor for chronic kidney disease and nonalcoholic fatty liver disease. Recent studies identify mechanisms common to both disease linked through an interorgan communication orchestrated by Fetuin-A, Adiponectin and 5'-AMP activated protein kinase ( AMPK). In liver and kidney, the energy sensor 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 common sequelae of obesity.%肥胖是肥胖相关性肾病和非酒精性脂肪肝病的重要危险因素。近年来研究表明，组织内的血清胎球蛋白A和脂联素，以及5'-AMP激活的蛋白激酶(AMPK)的协同作用是肥胖相关性肝肾疾病的共同机制，在肾脏足细胞和肝实质细胞的损伤中发挥枢纽作用，引发组织炎症、纤维化，以及终末期硬化。深入研究该早期共同通路，有助于发现肥胖相关性疾病治疗的新靶标。
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