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D-阿洛酮糖,D-果糖的差向异构体,可改善 Sprague-Dawley 大鼠的脂代谢。

D-psicose, an epimer of D-fructose, favorably alters lipid metabolism in Sprague-Dawley rats.

机构信息

†Department of Nutrition, University of Nagasaki, Siebold, 1-1-1 Manabino, Nagayo-cho, Nishisonogi-gun, Nagasaki 851-2195, Japan.

§Center for Industry, University and Government Cooperation, Nagasaki University, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan.

出版信息

J Agric Food Chem. 2015 Apr 1;63(12):3168-76. doi: 10.1021/jf502535p. Epub 2015 Mar 18.

DOI:10.1021/jf502535p
PMID:25754616
Abstract

D-Psicose, a C3 epimer of D-fructose, is known to lower body weight and adipose tissue weight and affect lipid metabolism. The precise mechanism remains unknown. It has been reported that D-psicose has a short half-life and is not metabolized in the body. To determine how D-psicose modifies lipid metabolism, rats were fed diets with or without 3% D-psicose for 4 weeks. Rats were decapitated without fasting every 6 h over a period of 24 h. Changes in serum and liver lipid levels, liver enzyme activity, and gene expression were quantified in experiment 1. Rats fed D-psicose had significantly lower serum insulin and leptin levels. Liver enzyme activities involved in lipogenesis were significantly lowered by the D-psicose diet, whereas gene expression of a transcriptional modulator of fatty acid oxidation was enhanced. In experiment 2, feeding the D-psicose diet gave significantly lower body weight (389 ± 3 vs 426 ± 6 g, p < 0.05) and food intake (23.8 ± 0.2 vs 25.7 ± 0.4 g/day, p < 0.05) compared to the control diet. Rats fed the D-psicose diet gave significantly higher energy expenditure in the light period and fat oxidation in the dark period compared to rats fed the control diet, whereas carbohydrate oxidation was lower. In summary, these results indicate that the D-psicose diet decreases lipogenesis, increases fatty acid oxidation, and enhances 24 h energy expenditure, leading to d-psicose's potential for weight management.

摘要

D-阿洛酮糖,D-果糖的 C3 差向异构体,已知可降低体重和脂肪组织重量,并影响脂质代谢。确切的机制尚不清楚。据报道,D-阿洛酮糖半衰期短,在体内不会代谢。为了确定 D-阿洛酮糖如何改变脂质代谢,将大鼠用含有或不含有 3% D-阿洛酮糖的饮食喂养 4 周。大鼠在 24 小时内不禁食,每隔 6 小时断头一次。在实验 1 中定量了血清和肝脂质水平、肝酶活性和基因表达的变化。喂食 D-阿洛酮糖的大鼠血清胰岛素和瘦素水平显著降低。D-阿洛酮糖饮食显著降低了参与脂肪生成的肝酶活性,而脂肪酸氧化转录调节剂的基因表达增强。在实验 2 中,与对照饮食相比,喂食 D-阿洛酮糖饮食的大鼠体重(389±3 比 426±6 g,p<0.05)和食物摄入量(23.8±0.2 比 25.7±0.4 g/天,p<0.05)显著降低。与对照饮食相比,喂食 D-阿洛酮糖饮食的大鼠在亮期的能量消耗和暗期的脂肪氧化显著增加,而碳水化合物氧化降低。总之,这些结果表明 D-阿洛酮糖饮食可减少脂肪生成,增加脂肪酸氧化,并增强 24 小时能量消耗,从而使 D-阿洛酮糖具有体重管理的潜力。

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