Modification of metabolic effects of ethanol by fructose.
Modification of metabolic effects of ethanol by fructose.
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果糖改变乙醇的代谢作用。
DOI：
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发表时间：
2009
期刊：
影响因子：
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通讯作者：
I. Hassinen
中科院分区：
文献类型：
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作者：
R. Ylikahri;M. Kähönen;I. Hassinen
.本文综述了果糖和乙醇在人和实验动物体内代谢相互作用的研究进展。这些相互作用的可能的生化机制被认为是。包括果糖和乙醇对碳水化合物和脂质代谢的影响的一些新的数据。
果糖增加乙醇对肝脏乳酸/丙酮酸和α-甘油磷酸/磷酸二羟丙酮比率的影响。因此，它增强了乙醇的基本代谢作用，即降低肝脏氧化还原状态。
酒精引起的肝内α-甘油磷酸浓度升高被认为是急性酒精性脂肪肝发病机制中的重要因素。但是，尽管果糖引起高甘油三酯血症并增强乙醇对肝脏α-甘油磷酸盐浓度的影响，但发现它减少了乙醇诱导的肝脏中甘油三酯的积累。葡萄糖也有类似的效果。其原因尚不确定，但果糖和葡萄糖对外周脂解的抑制可能是部分原因。
乙醇对碳水化合物代谢最重要的影响是通过过量产生NADH来抑制肝脏的再生。虽然果糖产生葡萄糖并不直接依赖于肝脏的氧化还原状态，但在体外乙醇会轻微抑制葡萄糖的产生。然而，即使在乙醇氧化过程中，体内果糖也能有效地转化为葡萄糖，在乙醇诱导的低血糖中，果糖能迅速恢复血糖水平。
. Present knowledge of the metabolic interactions between fructose and ethanol in man and laboratory animals is reviewed. The possible biochemical mechanisms of these interactions are considered. Some new data on the effects of fructose and ethanol on carbohydrate and lipid metabolism are included.
Fructose increases the effects of ethanol on the hepatic lactate/pyruvate and a-glycerophosphate/dihydroxyacetone phosphate ratios. Thus it augments the basic metabolic effect of ethanol, i.e. reduction of the hepatic redox state.
The ethanol-induced increase in hepatic a-glycerophosphate concentration has been regarded as an important factor in the pathogenesis of the acute alcoholic fatty liver. But although fructose causes hypertriglyceridaemia and augments the effect of ethanol on hepatic a-glycerophosphate concentration, it was found to diminish the ethanol-induced accumulation of triglycerides in the liver. Glucose had a similar effect. The reason for this is uncertain, but the inhibition of peripheral lipolysis by fructose and glucose might be partly responsible.
The most important effect of ethanol on carbohydrate metabolism is to inhibit hepatic gluconeogenesis by producing NADH in excess. Although the production of glucose from fructose is not directly dependent on the redox state of the liver, it is slightly inhibited by ethanol in vitro. However, in vivo fructose is effectively converted to glucose even during ethanol oxidation, and in ethanol-induced hypoglycaemia it rapidly restores the blood glucose level.