Mayes P A
Department of Veterinary Basic Sciences, Royal Veterinary College, University of London, UK.
Am J Clin Nutr. 1993 Nov;58(5 Suppl):754S-765S. doi: 10.1093/ajcn/58.5.754S.
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.
果糖的大多数代谢效应归因于肝脏对其的快速利用以及它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。这些影响包括肝脏中丙酮酸和乳酸生成立即增加、丙酮酸脱氢酶激活，以及非酯化脂肪酸从氧化向酯化的平衡转变，导致极低密度脂蛋白（VLDL）分泌增加。长期摄入果糖会增强这些效应，它会引起酶适应性变化，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。肝脏急性摄入果糖会使无机磷酸在果糖-1-磷酸中螯合，减少ATP合成。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，随之出现高尿酸血症。这些效应对于潜在的高甘油三酯血症或高尿酸血症个体尤为重要。
