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目的:探讨非肥胖(体质指数≤25)的原发性高血压(EH)患者脂肪细胞因子水平和应用罗格列酮(ROS)治疗后血压及脂肪细胞因子的变化,探讨ROS作用于EH患者的可能机制。方法:轻、中度,体质指数≤25的EH患者102例(EH组),在治疗开始时随机将上述患者分为ROS亚组及常规药物治疗亚组。另入选同期门诊体检健康者30例作为健康对照组。所有入选者于开始用药前及结束时空腹采2份静脉血标本,并行血压测量,血糖、血浆胰岛素测定,计算胰岛素敏感指数以及测定3种脂肪细胞因子:脂联素、瘦素、肿瘤坏死因子-α(TNF-α)。结果:与健康对照组相比,EH组脂联素水平明显减低,瘦素和TNF-α水平明显增高(P<0·05)。同治疗开始前比较,ROS亚组脂联素水平显著升高,TNF-α水平和血压显著下降(P<0·05);常规药物治疗亚组脂联素略有增高(P>0·05),TNF-α水平和血压明显减低(P<0·05)。与常规药物治疗亚组比较,ROS亚组脂联素水平显著升高(P<0·05),TNF-α水平、血压和血糖略低;2亚组间瘦素水平差异无统计学意义。结论:EH患者较健康者脂联素水平明显减低,瘦素和TNF-α水平明显增高;降压治疗可使EH患者脂联素水平升高,TNF-α水平明显降低;在降压药物基础上加用ROS可进一步提高脂联素水平,改善降压效果。
Objective: To investigate the changes of adipokines and adiponectin levels in non-obese (essential body mass index ≤25) patients with essential hypertension (EH) and the changes of blood pressure and adipocytokines after treatment with rosiglitazone (ROS) Possible mechanism. Methods: EH patients (mild to moderate) with body mass index ≤25 (EH group), 102 patients were randomly divided into two groups: the ROS subgroup and the conventional drug treatment subgroup. In the same period, 30 outpatients were selected as healthy control group. All participants received two fasting venous blood samples before and at the end of their medication. Parallel blood pressure measurements, blood glucose, and plasma insulin measurements were performed to calculate the insulin sensitivity index and to determine three adipocytokines: adiponectin, leptin, tumor necrosis factor -α (TNF-α). Results: Compared with healthy control group, adiponectin level was significantly decreased and leptin and TNF-α levels were significantly increased in EH group (P <0.05). Compared with those before treatment, adiponectin level was significantly increased in ROS subgroup, and TNF-α level and blood pressure were significantly decreased (P <0.05); Adiponectin in subgroup was slightly increased (P> 0.05) ), TNF-α level and blood pressure decreased significantly (P <0.05). The level of adiponectin in ROS subgroup was significantly higher than that in routine drug treatment subgroup (P <0.05). The level of TNF-α, blood pressure and blood sugar were slightly lower. There was no significant difference in leptin level between two subgroups. Conclusions: The levels of adiponectin in patients with EH are significantly lower than those in healthy controls, and the levels of leptin and TNF-α are significantly increased. Antihypertensive treatment can increase adiponectin level and TNF-α level in EH patients. Addition of ROS can further increase the level of adiponectin to improve antihypertensive effect.