《生命科学》 2017, 29(8): 790-796
摘 要：摘 要：果糖摄入量的增加与肥胖及非酒精性脂肪肝的严重程度密切相关。机体的果糖代谢在很多方面均与葡萄糖代谢不同。首先，果糖可促进食物摄取、减慢静息状态能量代谢。其次，在不增加能量摄入的条件下，果糖可绕过糖酵解途径中受细胞能量状态调控的关键限速步骤，生成过量的乙酰辅酶A，进入脂肪从头合成途径合成脂肪。但最重要的不同是，果糖在细胞内代谢时可引起快速而不可逆的ATP 消耗和嘌呤核苷酸转换，并最终诱导尿酸生成。果糖诱导的尿酸生成可减少脂肪酸氧化，尤其是可通过诱导线粒体氧化应激激活脂肪合成途径，导致肥胖和内脏脂肪蓄积。因此，果糖的特殊代谢效应可能在肥胖和内脏脂肪蓄积中扮演了重要角色，果糖摄入量增加可能是肥胖及其相关代谢性疾病的重要原因。
Abstract: Abstract: A high intake of fructose correlates closely with the degree of severity of obesity and non-alcoholic fatty liver disease (NAFLD). This may be accounted for by the metabolic differences between fructose and glucose. Firstly， fructose may stimulate food intake and reduce resting energy expenditure. Secondly， by avoiding the phosphofructokinase step in glycolysis which is tightly regulated by the cell energy status， a large proportion of fructose is converted to surplus acetyl-CoA independent of excessive energy intake. A large amount of surplus acetyl-CoA enters de novo lipogenesis and leads to formation of fatty acids. In particular， when fructose is metabolized in cells， ATP depletion and nucleotide turnover occur rapidly and irreversibly， and uric acid is eventually generated. Fructose-mediated uric acid generation can cause a reduction in fatty acid oxidation， but more importantly it can stimulate lipogenesis by inducing mitochondrial oxidative stress. Therefore， the unique aspects of fructose metabolism may have an important role in obesity and visceral fat accumulation. A high intake of fructose may increase the risk for obesity and obesity-related metabolic diseases.
