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说明：
关键词： 胰岛素抵抗,游离脂肪酸(FFA),型糖尿病
胰岛素抵抗的本质就是单位胰岛素的生物效应的降低，即胰岛素刺激葡萄糖利用能力的降低。最初，可以通过代偿性增加胰岛素分泌，产生高胰岛素血症，维持血糖水平正常。当这一过程发展到超过机体代偿极限，则表现为糖尿病。肥胖和2型糖尿病人中，普遍存在着胰岛素抵抗，这一点已从单纯性肥胖到肥胖性糖尿病患者的一系列研究中得到证实。可以说，胰岛素抵抗贯穿于2型糖尿病的整个发生、发展过程中。不仅表现在外周组织(即葡萄糖摄取的降低)，而且还表现在肝脏(即肝糖输出的增加)。然而胰岛素抵抗的机制，目前并不十分清楚。近年来认为游离脂肪酸(free fatty acid, FFA)在致胰岛素抵抗中占有重要地位。
一、FFA在胰岛素抵抗相关疾病中升高
正常生理条件下，脂肪分解产生的FFA由脂肪细胞释出进入血循环。而不同状态下，FFA氧化的量可以呈现出很大的差异。在肥胖者，尤其是腹型肥胖情况下，存在着脂肪代谢紊乱。脂肪的堆积，导致脂肪分解的活跃，大量FFA进入血液，产生高FFA血症。肥胖病人在血脂正常时，FFA已经升高，表明在反映机体脂代谢情况方面，FFA的变化比甘油三酯和胆固醇脂的变化更敏感。而且研究已证实2型糖尿病中，甘油三酯升高是独立于年龄和体重的危险因子。由此可以看出，FFA升高与胰岛素抵抗产生有着密切的联系。
目录：
一、FFA在胰岛素抵抗相关疾病中升高
二、FFA抑制外周葡萄糖的利用
三、FFA促进糖异生
四、FFA引起高胰岛素血症
五、降低FFA的途径及对胰岛素抵抗的影响
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