Translational Medicine Division, Department of Medicine, Federal University of São Paulo, São Paulo, SP, Brazil.
Renal, Cardiovascular and Metabolic Physiopharmacology Laboratory, Health and Biological Science Center, Mackenzie University, Rua da Consolacao, 930, São Paulo, SP, 01302-907, Brazil.
Eur J Nutr. 2016 Feb;55(1):83-91. doi: 10.1007/s00394-014-0826-5. Epub 2015 Jan 7.
Metabolic syndrome (MS) increases the risk of type 2 diabetes and cardiovascular disease. High consumption of fructose is a proposed cause of increased MS, manifested through hypertension, obesity, insulin resistance, and dyslipidemia. High NaCl also increases the risk of CD. The purpose of this study is to evaluate the influence of fructose and sodium on autonomic dysfunction and its relation with CD in MS. Fructose overload was started at weaning and continued through adulthood.
Male Wistar rats (21 days) were divided into four groups: Control (C), fructose consumption (10%, F), NaCl consumption (salt 1% for the 10 last days, S), and fructose and NaCl (FS), and monitored for 8 weeks. Metabolic evaluations consisted of Lee index, glycemia, insulin and glucose tolerance tests, triglycerides, and total cholesterol measurements. Cardiovascular parameters measured were arterial pressure (AP) and cardiac function performed by echocardiography. They also measured the influence of renin angiotensin (RAS) and autonomic nervous systems by drug blockage with losartan, atropine, and atenolol.
Energy analysis showed no change between groups. Fructose overload induced a MS state, confirmed by insulin resistance, glucose intolerance, and dyslipidemia. Fasting glucose was increased in F and FS rat groups compared with C and S groups. AP was higher in F, S, and FS groups in comparison with the C group. The hypotensive response after sympathetic blockade was increased in F, S, and FS versus C. The cardiac vagal tonus was reduced in F and FS animal groups. The intrinsic heart rate was decreased in the FS group (372 ± 9 bpm) compared with the C group (410 ± 13 bpm). The morphometric measurements evaluated through left ventricular diameter during diastole and the left ventricular diameter during systole decreased in the FS group (16 and 26%, respectively). Diastolic function was reduced in F and FS. The depressor response induced by losartan was increased in the F group in comparison with other groups. However, there was a uniform increase in plasma ACE activity in all treated groups compared with the C group.
Data suggest that early exposure to high fructose intake produced marked alterations in metabolic and cardiovascular function. When stimulated by NaCl, the fructose-fed subjects showed further impairment in cardiac function.
代谢综合征（MS）会增加 2 型糖尿病和心血管疾病的风险。高果糖摄入量被认为是 MS 增加的一个原因，其表现为高血压、肥胖、胰岛素抵抗和血脂异常。高盐也会增加 CD 的风险。本研究的目的是评估果糖和钠对自主神经功能障碍的影响及其与 MS 中 CD 的关系。在断奶后开始给果糖超负荷，并持续到成年期。
雄性 Wistar 大鼠（21 天）分为四组：对照组（C）、果糖组（10%，F）、盐组（1%盐摄入 10 天，S）和果糖和盐组（FS），并监测 8 周。代谢评估包括 Lee 指数、血糖、胰岛素和葡萄糖耐量试验、甘油三酯和总胆固醇测量。心血管参数测量包括动脉压（AP）和超声心动图进行的心脏功能。还通过使用氯沙坦、阿托品和阿替洛尔进行药物阻断来测量肾素-血管紧张素（RAS）和自主神经系统的影响。
能量分析显示各组之间没有变化。果糖超负荷导致胰岛素抵抗、葡萄糖不耐受和血脂异常，从而导致 MS 状态。与 C 组和 S 组相比，F 组和 FS 组的空腹血糖升高。与 C 组相比，F 组、S 组和 FS 组的 AP 更高。与 C 组相比，F、S 和 FS 组交感神经阻断后的降压反应增加。F 组和 FS 组的心脏迷走神经张力降低。FS 组的固有心率（372±9 bpm）低于 C 组（410±13 bpm）。FS 组左心室舒张直径（16%）和左心室收缩直径（26%）的形态学测量值降低。F 组和 FS 组舒张功能降低。与其他组相比，F 组洛沙坦诱导的降压反应增加。然而，与 C 组相比，所有治疗组的血浆 ACE 活性均均匀增加。
数据表明，早期暴露于高果糖摄入会导致代谢和心血管功能明显改变。当受到 NaCl 刺激时，果糖喂养的受试者的心脏功能进一步受损。
