Jürgens Hella, Haass Wiltrud, Castañeda Tamara R, Schürmann Annette, Koebnick Corinna, Dombrowski Frank, Otto Bärbel, Nawrocki Andrea R, Scherer Philipp E, Spranger Jochen, Ristow Michael, Joost Hans-Georg, Havel Peter J, Tschöp Matthias H
Department of Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany.
Obes Res. 2005 Jul;13(7):1146-56. doi: 10.1038/oby.2005.136.
The marked increase in the prevalence of obesity in the United States has recently been attributed to the increased fructose consumption. To determine if and how fructose might promote obesity in an animal model, we measured body composition, energy intake, energy expenditure, substrate oxidation, and several endocrine parameters related to energy homeostasis in mice consuming fructose.
We compared the effects of ad libitum access to fructose (15% solution in water), sucrose (10%, popular soft drink), and artificial sweetener (0% calories, popular diet soft drink) on adipogenesis and energy metabolism in mice.
Exposure to fructose water increased adiposity, whereas increased fat mass after consumption of soft drinks or diet soft drinks did not reach statistical significance (n = 9 each group). Total intake of energy was unaltered, because mice proportionally reduced their caloric intake from chow. There was a trend toward reduced energy expenditure and increased respiratory quotient, albeit not significant, in the fructose group. Furthermore, fructose produced a hepatic lipid accumulation with a characteristic pericentral pattern.
These data are compatible with the conclusion that a high intake of fructose selectively enhances adipogenesis, possibly through a shift of substrate use to lipogenesis.
美国肥胖患病率显著上升,近期被归因于果糖摄入量增加。为了确定果糖是否以及如何在动物模型中促进肥胖,我们测量了食用果糖的小鼠的身体组成、能量摄入、能量消耗、底物氧化以及与能量稳态相关的几个内分泌参数。
我们比较了随意摄入果糖(水中15%溶液)、蔗糖(10%,普通软饮料)和人工甜味剂(0卡路里,普通低糖软饮料)对小鼠脂肪生成和能量代谢的影响。
饮用果糖水会增加肥胖程度,而饮用软饮料或低糖软饮料后脂肪量增加未达到统计学显著性(每组n = 9)。能量总摄入量未改变,因为小鼠会相应减少其从食物中摄入的热量。果糖组存在能量消耗减少和呼吸商增加的趋势,尽管不显著。此外,果糖会导致肝脏脂质蓄积,并呈现特征性的中央周围模式。
这些数据支持以下结论,即高果糖摄入量可能通过将底物利用转向脂肪生成,选择性地增强脂肪生成。