Fructose, insulin resistance, and metabolic dyslipidemia.
Fructose, insulin resistance, and metabolic dyslipidemia.
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DOI：
10.1186/1743-7075-2-5
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发表时间：
2005-02-21
影响因子：
4.5
通讯作者：
Adeli, Khosrow
中科院分区：
文献类型：
--
作者：
Basciano, Heather;Federico, Lisa;Adeli, Khosrow
肥胖和2型糖尿病在美国和世界许多地方都以流行病的速度发生。“肥胖流行病”似乎主要是由于我们饮食的变化和体力活动的减少而出现的。一个重要但未得到充分重视的饮食变化是，由于大量摄入蔗糖和高果糖玉米糖浆（食品工业中常用的甜味剂），膳食果糖消费量大幅增加。高通量的果糖进入肝脏（能够代谢这种简单碳水化合物的主要器官）扰乱葡萄糖代谢和葡萄糖摄取途径，并导致从头脂肪生成和甘油三酯（TG）合成的速率显著增强，这是由来自果糖催化剂的TG分子的甘油和酰基部分的高通量驱动的。这些代谢紊乱似乎是在人类和动物模型中用高果糖喂养通常观察到的胰岛素抵抗诱导的基础。果糖诱导的胰岛素抵抗状态通常以严重的代谢性血脂异常为特征，这似乎是由肝和肠过度产生致动脉粥样硬化脂蛋白颗粒引起的。因此，最近流行病学和生物化学研究的新证据清楚地表明，果糖的高膳食摄入量已迅速成为代谢综合征发展的重要致病因素。迫切需要提高公众对与高果糖消费相关的风险的认识，并应做出更大努力，以遏制用高果糖添加剂补充包装食品。本综述将讨论果糖消费的趋势，增加果糖摄入的代谢后果，以及导致果糖诱导的脂肪生成，胰岛素抵抗和代谢性血脂异常的分子机制。
Obesity and type 2 diabetes are occurring at epidemic rates in the United States and many parts of the world. The "obesity epidemic" appears to have emerged largely from changes in our diet and reduced physical activity. An important but not well-appreciated dietary change has been the substantial increase in the amount of dietary fructose consumption from high intake of sucrose and high fructose corn syrup, a common sweetener used in the food industry. A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism. These metabolic disturbances appear to underlie the induction of insulin resistance commonly observed with high fructose feeding in both humans and animal models. Fructose-induced insulin resistant states are commonly characterized by a profound metabolic dyslipidemia, which appears to result from hepatic and intestinal overproduction of atherogenic lipoprotein particles. Thus, emerging evidence from recent epidemiological and biochemical studies clearly suggests that the high dietary intake of fructose has rapidly become an important causative factor in the development of the metabolic syndrome. There is an urgent need for increased public awareness of the risks associated with high fructose consumption and greater efforts should be made to curb the supplementation of packaged foods with high fructose additives. The present review will discuss the trends in fructose consumption, the metabolic consequences of increased fructose intake, and the molecular mechanisms leading to fructose-induced lipogenesis, insulin resistance and metabolic dyslipidemia.