Studies of the mechanism of fructose-induced hypertriglyceridemia in the rat.
Studies of the mechanism of fructose-induced hypertriglyceridemia in the rat.
复制标题
果糖诱导大鼠高甘油三酯血症机制的研究。
DOI：
10.1016/0026-0495(82)90155-x
复制
发表时间：
1982
期刊：
影响因子：
--
通讯作者：
G. Reaven
中科院分区：
文献类型：
--
作者：
I. Zavaroni;I. Zavaroni;Yli;Yli;G. Reaven;G. Reaven
碳水化合物诱导的高胆固醇血症在大鼠中很容易产生，而果糖在这方面表现出特别强的作用。在这项研究中，我们比较了高果糖或葡萄糖（占总热量的66%）饮食对大鼠碳水化合物和脂质代谢各个方面的影响。结果证实了之前的观察结果，即果糖（456 ± 276 mg/dl）更有效（p< 0.001）在升高血浆TG浓度方面，（242 ± 13 mg/dl），表明两种碳水化合物引起的高脂血症程度的差异与试验饮食增加VLDL-TG分泌的能力密切相关（r= 0.85，p < 0.001）。葡萄糖和果糖喂养导致相当程度的高胰岛素血症，血浆TG浓度增加之前，高胰岛素血症在果糖喂养的大鼠。因此，可以得出结论，果糖可以直接作用于肝脏以增加VLDL-TG分泌，并且果糖诱导的高甘油三酯血症可以在没有高胰岛素血症的情况下发生。另一方面，在运动训练的大鼠中，果糖产生的血浆TG浓度的升高显著降低，这与血浆胰岛素浓度的降低有关。基于这些观察结果，我们认为果糖喂养通过直接刺激肝脏VLDL-TG分泌以及通过产生胰岛素抵抗和高胰岛素血症来产生高胰岛素血症，并且这是这两种单独作用的组合效应，其解释了果糖诱导的高胰岛素血症的幅度。
Carbohydrate-induced hypertriglyceridemia is easily produced in the rat, and fructose has been shown to be particularly potent in this regard. In this study we have compared the effects of feeding rats diets high (66% of total calories) in fructose or glucose on various aspects of carbohydrate and lipid metabolism. The results confirmed previous observations that fructose (456 ± 276 mg/dl) was more potent (p< 0.001) in raising plasma TG concentration than was glucose (242 ± 13 mg/dl), and indicated that the difference in magnitude of hypertriglyceridemia produced by the two carbohydrates was closely related to the ability of the test diets to increase VLDL-TG secretion (r= 0.85,p< 0.001). Both glucose and fructose feeding led to comparable degrees of hyperinsulinemia, and plasma TG concentrations increased before hyperinsulinemia evolved in fructose-fed rats. Therefore, it was concluded that fructose can act directly on the liver to increase VLDL-TG secretion, and that fructose-induced hypertriglyceridemia can occur in the absence of hyperinsulinemia. On the other hand, the rise in plasma TG concentration produced by fructose was reduced dramatically in exercise-trained rats, and this was associated with a decrease in plasma insulin concentration. Based upon these observations, we suggest that fructose feeding produces hypertriglyceridemia by directly stimulating hepatic VLDL-TG secretion, as well as by producing insulin resistance and hyperinsulinemia, and that it is the combined effect of these two separate actions which accounts for the magnitude of fructose-induced hypertriglyceridemia.