Intermediary metabolism of fructose

Intermediary metabolism of fructose
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DOI:
10.1093/ajcn/58.5.754s
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发表时间:
1993-01-01
影响因子:
7.1
通讯作者:
Mayes, Peter A.
Mayes, Peter A.
中科院分区:
医学1区
文献类型:
--
作者:
Mayes, Peter A.

文献摘要

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果糖的大部分代谢作用是由于其被肝脏快速利用,并绕过糖酵解中的磷酸果糖激酶调节步骤,从而对碳水化合物和脂质代谢产生深远影响。这些后果包括肝脏丙酮酸和乳酸生成的立即增加,丙酮酸脱氢酶的激活,以及非酯化脂肪酸从氧化到酯化的平衡转变,导致极低密度脂蛋白(VLDL)的分泌增加。果糖的长期吸收增强了这些影响,导致酶适应,增加脂肪生成和VLDL分泌,导致甘油三酯血症、葡萄糖耐量降低和高胰岛素血症。肝脏对果糖的急性负荷导致果糖-1-磷酸中无机磷酸盐的隔离和ATP合成的减少。因此,ATP对腺嘌呤核苷酸降解酶的抑制作用被消除,尿酸形成加速,导致高尿酸血症。这些影响对潜在的高甘油三酯血症或高尿酸血症患者特别重要。
Most of the metabolic effects of fructose are due to its rapid utilization by the liver and it by-passing the phosphofructokinase regulatory step in glycolysis, leading to far reaching consequences to carbohydrate and lipid metabolism. These consequences include immediate hepatic increases in pyruvate and lactate production, activation of pyruvate dehydrogenase, and a shift in balance from oxidation to esterification of nonesterified fatty acids, resulting in increased secretion of very-low-density-lipoprotein (VLDL). These effects are augmented by long-term absorption of fructose, which causes enzyme adaptations that increase lipogenesis and VLDL secretion, leading to triglyceridemia, decreased glucose tolerance, and hyperinsulinemia. Acute loading of the liver with fructose causes sequestration of inorganic phosphate in fructose-1-phosphate and diminished ATP synthesis. Consequently, the inhibition by ATP of the enzymes of adenine nucleotide degradation is removed and uric acid formation accelerates with consequent hyperuricemia. These effects are of particular significance to potentially hypertriglyceridemic or hyperuricemic individuals.