脂联素是一种脂肪因子，具有抗糖尿病、抗心血管疾病、抗动脉粥样硬化、抗炎症反应等多种生物效应。然而脂联素信号通路在肝脏脂肪变性中的作用及机制仍不清楚。我们的前期研究发现TCTP(Translationally Controlled Tumor Protein)为脂联素信号通路中的新的负性调节蛋白，且高脂诱导肝脏中TCTP表达升高，特异性敲除小鼠肝脏TCTP基因抵抗高脂饮食诱导的肝脏脂肪变性和胰岛素抵抗。基于以上重要发现，我们认为肝脏TCTP表达的升高可能是肥胖导致肝细胞脂肪变性及其引起的代谢失衡的一个重要因素。在本课题中，我们将利用独特的细胞和动物模型，阐明TCTP和脂联素信号通路在调控肝脂代谢稳态的作用与机制。通过本研究，明确TCTP能否作为治疗肝脏脂肪变性的新型靶标蛋白。

Adiponectin is a well-known insulin sensitizer that suppresses glucose production from the liver, one of the major target tissues of adiponectin action. But the relationship between adiponectin signaling and liver steatosis remain largely unknown.To address the aforementioned questions, we screened a yeast two-hybrid cDNA library using APPL2 as bait. This screening led to the identification of an APPL2 interacting protein, TCTP (Translationally Controlled Tumor Protein). TCTP protein levels were significantly higher in the liver of diet-induced obese mice compared to lean controls. In addition, liver-specific disruption of TCTP expression improved glucose metabolism and increased resistance to diet-induced obesity and hepatosteatosis. Based on these findings, we hypothesize that TCTP, plays a key role in the negative regulation of adiponectin signaling and hepatosteatosis.