title: Dietary D-psicose reduced visceral fat mass in high-fat diet-induced obese rats.
abstract: D-Psicose, a C-3 epimer of D-fructose, has shown promise in reducing body fat accumulation in normal rats and plasma glucose level in genetic diabetic mice. Effects of D-psicose on diet-induced obesity are not clearly elucidated, and we investigated food intake, body weight, and fat accumulation in rats fed high-fat (HF) diet. Sprague-Dawley rats became obese by feeding HF diet for 4 wk, and were assigned either to normal or HF diet supplemented with or without D-psicose, sucrose, or erythritol for 8 wk. Changing HF to normal diet gained less body weight and adipose tissue due to different energy intake. D-psicose-fed rats exhibited lower weight gain, food efficiency ratio, and fat accumulation than erythritol- and sucrose-fed rats. This effect was more prominent in D-psicose-fed rats with normal diet than with HF diet, suggesting combination of psicose and calorie restriction further reduced obesity. There was no difference in serum cholesterol/high-density lipoprotein (HDL)-C and low-density lipoprotein (LDL)-C/HDL-C ratios between D-psicose group and other groups. Liver weight in 5% psicose group with normal diet was higher than in other groups, but histopathological examination did not reveal any psicose-related change. D-Psicose inhibited the differentiation of mesenchymal stem cell (MSC) to adipose tissue in a concentration-dependent manner. These results demonstrate that D-psicose produces a marked decrease, greater than erythritol, in weight gain and visceral fat in an established obesity model by inhibiting MSC differentiation to adipocyte. Thus, D-psicose can be useful in preventing and reducing obesity as a sugar substitute and food ingredient.
  
  
  CONCLUSIONS
  We can develop D-psicose as a sugar substitute and food ingredient since it can prevent obesity in normal people, but also suppress adiposity as a sugar substitute or food ingredients with antiobesity effect in obese people. D-psicose can be unique functional sweetener because of its function of reducing visceral fat mass and weight gain.
authors.affiliation: Pharmaceutical Research Inst, CJ CheilJedang Corp, Ichon, Kyonggi-do 467-812, Korea.
authors.forename: Young-Mee
authors.initials: YM
authors.lastname: Chung
authors.forename: Joo
authors.initials: J
authors.lastname: Hyun Lee
authors.forename: Deuk
authors.initials: D
authors.lastname: Youl Kim
authors.forename: Se-Hee
authors.initials: SH
authors.lastname: Hwang
authors.forename: Young-Ho
authors.initials: YH
authors.lastname: Hong
authors.forename: Seong-Bo
authors.initials: SB
authors.lastname: Kim
authors.forename: Song
authors.initials: S
authors.lastname: Jin Lee
authors.forename: Chi
authors.initials: C
authors.lastname: Hye Park
mesh_terms: D017667:Adipocytes / Q000187:drug effects; D000818:Animals; D001823:Body Composition / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D059305:Diet, High-Fat / Q000009:adverse effects*; D019587:Dietary Supplements; D002149:Energy Intake / Q000187:drug effects; D005632:Fructose / Q000008:administration & dosage*; D050152:Intra-Abdominal Fat / Q000187:drug effects*; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D009765:Obesity / Q000178:diet therapy* / Q000209:etiology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; C003243:psicose; D005632:Fructose