空腹血糖升高是2型糖尿病的重要特征，最新研究发现白色脂肪组织分解引起的肝脏乙酰辅酶A升高，是导致肝糖异生增加、进而升高2型糖尿病空腹血糖的重要原因。AdipoRon是脂联素受体激动剂，可改善2型糖尿病，但AdipoRon是否作用于白色脂肪组织缓解2型糖尿病还未见报道。前期研究发现AdipoRon治疗可减少肥胖小鼠的脂肪组织分解、降低肝脏乙酰辅酶A和空腹血糖。基于预实验和文献调研，我们推测AdipoRon可能抑制白色脂肪组织分解，减少进入肝脏的游离脂肪酸和甘油，进而降低肝脏乙酰辅酶A浓度和丙酮酸羧化酶活性，最终抑制肝糖异生、降低2型糖尿病空腹血糖。本研究拟应用自发性2型糖尿病Zucker肥胖大鼠和原代分离的脂肪细胞、稳定同位素体内示踪技术、高胰岛素正葡萄糖钳夹实验及糖脂代谢通量的精确计算方法，揭示AdipoRon治疗2型糖尿病的新机制，为阐明2型糖尿的发病机制和药物防治提供重要实验依据。

Type 2 diabetes is characterized by elevated fasting blood glucose. Recent studies have found that increased white adipose tissue-derived hepatic Acetyl-CoA, is an important cause of increased hepatic gluconeogenesis and thus elevated fasting blood glucose in type 2 diabetes. AdipoRon is an adiponectin receptor agonist. Previous studies have shown that AdipoRon can act on liver and skeletal muscle tissue to improve insulin resistance in the treatment of type 2 diabetes, but whether AdipoRon can alleviate type 2 diabetes by acting on white adipose tissue has not been reported. Our previous study found that AdipoRon treatment can reduce white adipose tissue lipolysis, lower hepatic Acetyl-CoA concentration and fasting blood glucose in high fat diet-fed mice. Based on preliminary experiments and literature research, we hypothesize that AdipoRon may act on white adipose tissue, inhibit adipose tissue lipolysis, reduce free fatty acids and glycerol entering the liver, thereby reduce hepatic Acetyl CoA concentration and pyruvate carboxylase activity, and ultimately inhibit hepatic gluconeogenesis and fasting blood glucose in type 2 diabetes. In this study, we intend to apply Zucker diabetic fatty rats and primary isolated adipocytes, use a novel in vivo stable isotope tracer technique to accurately quantify glucose and lipid metabolic fluxes，and further reveal the potential new mechanism of AdipoRon in the treatment of type 2 diabetes. This work will provide an important experimental data for elucidating the pathogenesis and prevention of type 2 diabetes.