Adipokine chemerin plays important roles in disorders of glucose and lipid metabolism of obesity and obesity-related diseases, and exercise-induced improvement of glucose and lipid metabolism is closely related to the decrease of chemerin, but the mechanisms by which chemerin regulates glucose and lipid metabolism remain unclarified. Hypotestosterone induces male obesity and disorders of glucose and lipid metabolism through androgen receptor (AR) and its target genes: glucose and lipid metabolism-related molecules (including FOXO1, PEPCK, PGC-1α, and SCD1). Recently, the link between them has been reported that chemerin modulated the secretion of androgen. In this study, global chemerin knockout (chemerin (−/−)) mice were established to demonstrate the roles of chemerin in regulating blood glucose and blood lipid of mice under diet (high-fat (HFD) and normal diet) and exercise interventions and then to explore its mechanisms (AR – glucose and lipid metabolism enzymes). We found that the blood lipid and adipocyte size were low accompanied by the improvements in the levels of serum testosterone, gastrocnemius AR, and gastrocnemius FOXO1, SCD1, and PGC-1α in HFD chemerin (−/−) mice, but exercise-induced improvements of these indicators in HFD WT mice were attenuated or abolished in HFD chemerin (−/−) mice. In conclusion, the decrease of chemerin improved the blood lipid profile of HFD male mice at sedentary and exercise states, mediated partly by the increases of testosterone and AR to regulate glucose and lipid metabolism enzymes. To our knowledge, it is the first report that chemerin’s regulation of glucose and lipid metabolism might be mediated by testosterone and AR in vivo.

脂肪因子凯莫林在肥胖糖脂代谢紊乱及肥胖相关疾病中发挥着重要作用,运动引起的糖脂代谢改善与凯莫林的降低密切相关,但凯莫林调节糖脂代谢的机制仍不清楚。低睾酮通过雄激素受体（AR）及其靶基因：糖脂代谢相关分子（包括FOXO1、PEPCK、PGC-1α和SCD1）诱导男性肥胖和糖脂代谢紊乱。最近，据报道，它们之间的联系是凯莫瑞调节雄激素的分泌。在本研究中，建立了凯莫瑞全基因敲除小鼠（凯莫瑞（−/−）），以证明凯莫瑞在饮食（高脂（HFD）和正常饮食）和运动干预以及运动干预下对小鼠血糖和血脂的调节作用。然后探索其机制（AR - 葡萄糖和脂质代谢酶）。我们发现，HFD chemerin (−/−) 小鼠的血脂和脂肪细胞大小较低，同时血清睾酮、腓肠肌 AR 和腓肠肌 FOXO1、SCD1 和 PGC-1α 水平有所改善，但运动引起的改善HFD WT 小鼠中的这些指标在 HFD chemerin (−/−) 小鼠中减弱或消除。总之，凯莫瑞的减少改善了 HFD 雄性小鼠在久坐和运动状态下的血脂状况，部分是通过增加睾酮和 AR 来调节葡萄糖和脂质代谢酶来介导的。据我们所知，这是首次报道凯莫瑞在体内调节糖脂代谢可能是由睾酮和AR介导的。