Han Youngji, Han Hye Jin, Kim Ae-Hyang, Choi Ji-Young, Cho Su-Jung, Park Yong Bok, Jung Un Ju, Choi Myung-Sook
Department of Food Science and Nutrition, Kyungpook National University, Daegu, Republic of Korea.
Center for Food and Nutritional Genomics Research, Kyungpook National University, Daegu, Republic of Korea.
Mol Nutr Food Res. 2016 Jul;60(7):1695-706. doi: 10.1002/mnfr.201500771. Epub 2016 Apr 24.
A number of findings suggest that zero-calorie d-allulose, also known as d-psicose, has beneficial effects on obesity-related metabolic disturbances. However, it is unclear whether d-allulose can normalize the metabolic status of diet-induced obesity without having an impact on the energy density. We investigated whether 5% d-allulose supplementation in a high fat diet(HFD) could normalize body fat in a diet-induced obesity animal model under isocaloric pair-fed conditions.
Mice were fed an HFD with or without various sugar substitutes (d-glucose, d-fructose, erytritol, or d-allulose, n = 10 per group) for 16 wk. Body weight and fat-pad mass in the d-allulose group were dramatically lowered to that of the normal group with a simultaneous decrease in plasma leptin and resistin concentrations. d-allulose lowered plasma and hepatic lipids while elevating fecal lipids with a decrease in mRNA expression of CD36, ApoB48, FATP4, in the small intestine in mice. In the liver, activities of both fatty acid synthase and β-oxidation were downregulated by d-allulose to that of the normal group; however, in WAT, fatty acid synthase was decreased while β-oxidation activity was enhanced.
Taken together, our findings suggest that 5% dietary d-allulose led to the normalization of the metabolic status of diet-induced obesity by altering lipid-regulating enzyme activities and their gene-expression level along with fecal lipids.
多项研究结果表明,零热量的D-阿洛酮糖(也称为D- psicose)对肥胖相关的代谢紊乱具有有益作用。然而,尚不清楚D-阿洛酮糖能否在不影响能量密度的情况下使饮食诱导肥胖的代谢状态正常化。我们研究了在等热量配对喂养条件下,高脂饮食(HFD)中添加5%的D-阿洛酮糖是否能使饮食诱导肥胖动物模型的体脂正常化。
给小鼠喂食含或不含各种糖替代品(D-葡萄糖、D-果糖、赤藓糖醇或D-阿洛酮糖,每组n = 10)的高脂饮食16周。D-阿洛酮糖组的体重和脂肪垫质量显著降低至正常组水平,同时血浆瘦素和抵抗素浓度降低。D-阿洛酮糖降低了血浆和肝脏脂质水平,同时增加了粪便脂质水平,小鼠小肠中CD36、ApoB48、FATP4的mRNA表达降低。在肝脏中,脂肪酸合酶和β-氧化的活性均被D-阿洛酮糖下调至正常组水平;然而,在白色脂肪组织中,脂肪酸合酶减少而β-氧化活性增强。
综上所述,我们的研究结果表明,饮食中5%的D-阿洛酮糖通过改变脂质调节酶活性及其基因表达水平以及粪便脂质,使饮食诱导肥胖的代谢状态正常化。