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d ‐Allulose supplementation normalized the body weight and fat‐pad mass in diet‐induced obese mice via the regulation of lipid metabolism under isocaloric fed condition
Author(s) -
Han Youngji,
Han Hye Jin,
Kim AeHyang,
Choi JiYoung,
Cho SuJung,
Park Yong Bok,
Jung Un Ju,
Choi MyungSook
Publication year - 2016
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201500771
Subject(s) - medicine , endocrinology , fatty acid synthase , resistin , leptin , chemistry , lipid metabolism , diet induced obese , cd36 , obesity , biology , adipokine , receptor , insulin resistance
Scope 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.Methods and results 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.Conclusion 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.