Human Movement Laboratory, São Judas Tadeu University, São Paulo, Brazil.
Clinics (Sao Paulo). 2011;66(10):1793-6. doi: 10.1590/s1807-59322011001000019.
Because autonomic dysfunction has been found to lead to cardiometabolic disorders and because studies have reported that simvastatin treatment has neuroprotective effects, the objective of the present study was to investigate the effects of simvastatin treatment on cardiovascular and autonomic changes in fructose-fed female rats.
Female Wistar rats were divided into three groups: controls (n = 8), fructose (n = 8), and fructose+ simvastatin (n = 8). Fructose overload was induced by supplementing the drinking water with fructose (100 mg/L, 18 wks). Simvastatin treatment (5 mg/kg/day for 2 wks) was performed by gavage. The arterial pressure was recorded using a data acquisition system. Autonomic control was evaluated by pharmacological blockade.
Fructose overload induced an increase in the fasting blood glucose and triglyceride levels and insulin resistance. The constant rate of glucose disappearance during the insulin intolerance test was reduced in the fructose group (3.4 ± 0.32%/min) relative to that in the control group (4.4 ± 0.29%/min). Fructose + simvastatin rats exhibited increased insulin sensitivity (5.4 ± 0.66%/min). The fructose and fructose + simvastatin groups demonstrated an increase in the mean arterial pressure compared with controls rats (fructose: 124 ± 2 mmHg and fructose+simvastatin: 126 ± 3 mmHg vs. controls: 112 ± 2 mmHg). The sympathetic effect was enhanced in the fructose group (73 ± 7 bpm) compared with that in the control (48 ± 7 bpm) and fructose+simvastatin groups (31 ± 8 bpm). The vagal effect was increased in fructose + simvastatin animals (84 ± 7 bpm) compared with that in control (49 ± 9 bpm) and fructose animals (46 ± 5 bpm).
Simvastatin treatment improved insulin sensitivity and cardiac autonomic control in an experimental model of metabolic syndrome in female rats. These effects were independent of the improvements in the classical plasma lipid profile and of reductions in arterial pressure. These results support the hypothesis that statins reduce the cardiometabolic risk in females with metabolic syndrome.
由于自主神经功能障碍已被发现可导致心脏代谢紊乱，并且研究报告称辛伐他汀治疗具有神经保护作用，因此本研究的目的是探讨辛伐他汀治疗对果糖喂养雌性大鼠心血管和自主变化的影响。
将雌性 Wistar 大鼠分为三组：对照组（n=8）、果糖组（n=8）和果糖+辛伐他汀组（n=8）。通过在饮用水中添加果糖（100mg/L，18 周）诱导果糖超负荷。通过灌胃给予辛伐他汀治疗（5mg/kg/天，2 周）。使用数据采集系统记录动脉压。通过药理学阻断评估自主神经控制。
果糖超负荷导致空腹血糖和甘油三酯水平升高以及胰岛素抵抗。在胰岛素不耐受试验中，葡萄糖的恒速清除率在果糖组（3.4±0.32%/min）低于对照组（4.4±0.29%/min）。果糖+辛伐他汀组表现出胰岛素敏感性增加（5.4±0.66%/min）。与对照组相比，果糖组和果糖+辛伐他汀组的平均动脉压升高（果糖：124±2mmHg 和果糖+辛伐他汀：126±3mmHg 与对照组：112±2mmHg）。与对照组（48±7bpm）和果糖+辛伐他汀组（31±8bpm）相比，果糖组的交感神经效应增强（73±7bpm）。与对照组（49±9bpm）和果糖组（46±5bpm）相比，果糖+辛伐他汀动物的迷走神经效应增加（84±7bpm）。
辛伐他汀治疗改善了代谢综合征雌性大鼠实验模型中的胰岛素敏感性和心脏自主神经控制。这些作用独立于改善经典血浆脂质谱和降低动脉压。这些结果支持他汀类药物降低代谢综合征女性心血管代谢风险的假说。
