Swarbrick Michael M, Stanhope Kimber L, Elliott Sharon S, Graham James L, Krauss Ronald M, Christiansen Mark P, Griffen Steven C, Keim Nancy L, Havel Peter J
Department of Nutrition, University of California, Davis, CA 95616, USA.
Br J Nutr. 2008 Nov;100(5):947-52. doi: 10.1017/S0007114508968252.
Fructose consumption in the USA has increased over the past three decades. During this time, obesity, insulin resistance and the metabolic syndrome have also increased in prevalence. While diets high in fructose have been shown to promote insulin resistance and increase TAG concentrations in animals, there are insufficient data available regarding the long-term metabolic effects of fructose consumption in humans. The objective of the present study was to investigate the metabolic effects of 10-week consumption of fructose-sweetened beverages in human subjects under energy-balanced conditions in a controlled research setting. Following a 4-week weight-maintaining complex carbohydrate diet, seven overweight or obese (BMI 26.8-33.3 kg/m2) postmenopausal women were fed an isoenergetic intervention diet, which included a fructose-sweetened beverage with each meal, for 10 weeks. The intervention diet provided 15 % of energy from protein, 30 % from fat and 55 % from carbohydrate (30 % complex carbohydrate, 25 % fructose). Fasting and postprandial glucose, insulin, TAG and apoB concentrations were measured. Fructose consumption increased fasting glucose concentrations and decreased meal-associated glucose and insulin responses (P = 0.0002, P = 0.007 and P = 0.013, respectively). Moreover, after 10 weeks of fructose consumption, 14 h postprandial TAG profiles were significantly increased, with the area under the curve at 10 weeks being 141 % higher than at baseline (P = 0.04). Fructose also increased fasting apoB concentrations by 19 % (P = 0.043 v. baseline). In summary, consumption of fructose-sweetened beverages increased postprandial TAG and fasting apoB concentrations, and the present results suggest that long-term consumption of diets high in fructose could lead to an increased risk of CVD.
在过去三十年中，美国的果糖消费量有所增加。在此期间，肥胖症、胰岛素抵抗和代谢综合征的患病率也有所上升。虽然高果糖饮食已被证明会促进动物的胰岛素抵抗并增加甘油三酯（TAG）浓度，但关于人类食用果糖的长期代谢影响的数据不足。本研究的目的是在可控的研究环境中，调查能量平衡条件下人类受试者饮用10周果糖甜味饮料的代谢影响。在进行为期4周的维持体重的复合碳水化合物饮食后，7名超重或肥胖（体重指数26.8 - 33.3 kg/m²）的绝经后女性接受了等能量干预饮食，每餐都包含一种果糖甜味饮料，为期10周。干预饮食提供的能量中，15%来自蛋白质，30%来自脂肪，55%来自碳水化合物（30%为复合碳水化合物，25%为果糖）。测量了空腹和餐后的葡萄糖、胰岛素、TAG和载脂蛋白B（apoB）浓度。食用果糖会增加空腹血糖浓度，并降低与进餐相关的葡萄糖和胰岛素反应（分别为P = 0.0002、P = 0.007和P = 0.013）。此外，食用果糖10周后，餐后14小时的TAG曲线显著升高，10周时曲线下面积比基线高141%（P = 0.04）。果糖还使空腹apoB浓度增加了19%（与基线相比，P = 0.043）。总之，饮用果糖甜味饮料会增加餐后TAG和空腹apoB浓度，目前的结果表明，长期食用高果糖饮食可能会增加心血管疾病（CVD）的风险。
