目的 探讨左卡尼汀对高脂喂养大鼠棕色脂肪的影响及其相关机制。方法 将30只SD大鼠随机分为对照组、模型组和左卡尼汀低、中、高剂量（100、200、300 mg/kg）组，每组各6只。每日ig给药，治疗12周后称重、处死大鼠，收集血清和棕色脂肪组织，检测血清相关生化指标，测定棕色脂肪组织中解偶联蛋白1（UCP1）和磷酸化AKT（p-AKT）的表达水平。结果 与模型组相比，左卡尼汀100、200、300 mg/kg组的总胆固醇（TC）、三酰甘油（TG）明显降低，高密度脂蛋白胆固醇（HDL-C）明显升高（P<0.05）；左卡尼汀100、200 mg/kg组的体质量明显降低，棕色脂肪组织（BAT）质量、BAT质量/体质量明显升高（P<0.05）。与模型组相比，左卡尼汀100、200 mg/kg组BAT中UCP1 RNA明显增加，差异有统计学意义（P<0.05）。与模型组相比，左卡尼汀组100、200、300 mg/kg组BAT中UCP1和p-AKT蛋白表达明显增加，差异有统计学意义（P<0.05、0.01），且呈剂量相关性。结论 左卡尼汀具有降脂和促进棕色脂肪活化的作用，这可能与其增加棕色脂肪组织中UCP1和p-AKT的表达有关。

Objective To investigate the effects of L-evocarnitine on brown adipose tissue in obese rats and its related mechanism. Methods Thirty SD rats were randomly divided into control group, model group, and L-evocarnitine (100, 200, and 300 mg/kg) groups. Each group had 6 cases, and ig administration with drugs per day. After 12 weeks of treatment, rats were sacrificed for collection of serum and brown adipose tissue. The expression levels of uncoupling protein 1 (UCP1) and phosphorylated AKT (p-AKT) in brown adipose tissue were determined. Results Compared with the model group, TC and TG in L-evocarnitine 100, 200, and 300 mg/kg groups were significantly decreased (P<0.05), but HDL-C in L-evocarnitine 100 and 200, 300 mg/kg groups was significantly increased (P<0.05). Compared with the model group, the body weight in L-evocarnitine 100, 200 mg/kg groups were significantly decreased (P<0.05), but BAT weight and BAT weight/body weight were significantly increased (P<0.05). Compared with the model group, UCP1 RNA in L-evocarnitine 100 and 200 mg/kg groups was increased, with significant difference (P<0.05). Compared with the model group, UCP1 and p-AKT protein in L-evocarnitine 100, 200, and 300 mg/kg groups were significantly increased (P<0.05 and 0.01), with dose-dependent. Conclusion L-evocarnitine can reduce lipid and promote activation of brown adipose tissue, which may be related to its increasing expression of UCP1 and p-AKT in brown adipose tissue.

南京市卫生青年人才培养工程第三层次资助项目（QRX17173）；南京药学会常州四药医院药学科研基金资助项目（2019YX026）