title: Effects of a nonnutritive sweetener on body adiposity and energy metabolism in mice with diet-induced obesity.
abstract: OBJECTIVE
  Nonnutritive sweeteners (NNSs) have been studied in terms of their potential roles in type 2 diabetes, obesity, and related metabolic disorders. Several studies have suggested that NNSs have several specific effects on metabolism such as reduced postprandial hyperglycemia and insulin resistance. However, the detailed effects of NNSs on body adiposity and energy metabolism have not been fully elucidated. We investigated the effects of an NNS on energy metabolism in mice with diet-induced obesity (DIO).
  
  
  METHODS
  DIO mice were divided into NNS-administered (4% NNS in drinking water), sucrose-administered (33% sucrose in drinking water), and control (normal water) groups. After supplementation for 4 weeks, metabolic parameters, including uncoupling protein (UCP) levels and energy expenditure, were assessed.
  
  
  RESULTS
  Sucrose supplementation increased hyperglycemia, body adiposity, and body weight compared to the NNS-administered and control groups (P<0.05 for each). In addition, NNS supplementation decreased hyperglycemia compared to the sucrose-administered group (P<0.05). Interestingly, NNS supplementation increased body adiposity, which was accompanied by hyperinsulinemia, compared to controls (P<0.05 for each). NNS also increased leptin levels in white adipose tissue and triglyceride levels in tissues compared to controls (P<0.05 for each). Notably, compared to controls, NNS supplementation decreased the UCP1 level in brown adipose tissue and decreased O2 consumption in the dark phase.
  
  
  CONCLUSIONS
  NNSs may be good sugar substitutes for people with hyperglycemia, but appear to influence energy metabolism in DIO mice.
authors.affiliation: Department of Endocrinology and metabolism, Faculty of Medicine, Oita University, Yufu, Oita, 879-5593, Japan.
authors.forename: Kimihiko
authors.initials: K
authors.lastname: Mitsutomi
authors.forename: Takayuki
authors.initials: T
authors.lastname: Masaki
authors.forename: Takanobu
authors.initials: T
authors.lastname: Shimasaki
authors.forename: Koro
authors.initials: K
authors.lastname: Gotoh
authors.forename: Seiichi
authors.initials: S
authors.lastname: Chiba
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Kakuma
authors.forename: Hirotaka
authors.initials: H
authors.lastname: Shibata
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects*; D002001:Adipose Tissue, Brown / Q000378:metabolism; D052436:Adipose Tissue, White / Q000187:drug effects / Q000378:metabolism; D050154:Adiposity / Q000187:drug effects*; D000818:Animals; D004032:Diet; D004734:Energy Metabolism / Q000187:drug effects*; D006946:Hyperinsulinism / Q000139:chemically induced*; D007473:Ion Channels / Q000097:blood; D020738:Leptin / Q000378:metabolism; D051379:Mice; D024101:Mitochondrial Proteins / Q000097:blood; D009765:Obesity / Q000209:etiology / Q000378:metabolism*; D013395:Sucrose / Q000494:pharmacology; D013549:Sweetening Agents / Q000008:administration & dosage / Q000494:pharmacology*; D014280:Triglycerides / Q000378:metabolism; D000071256:Uncoupling Protein 1
chemical_list: D007473:Ion Channels; D020738:Leptin; D024101:Mitochondrial Proteins; D013549:Sweetening Agents; D014280:Triglycerides; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1; D013395:Sucrose
keywords: BAT; CPT-1; DIO; FAS; Leptin; MSL; NNS; NPY; Nonnutritive sweetener; Obesity; PGC-1; POMC; PPAR; TG; UCP; Uncoupling protein; WAT; brown adipose tissue; carnitine palmitoyltransferase 1; diet-induced obesity; fatty acid synthetase; neuropeptide Y; nonnutritive sweetener; peroxisome proliferator-activated receptor; peroxisome proliferator-activated receptor γ coactivator 1; proopiomelanocortin; skeletal muscle; triglyceride; uncoupling protein; white adipose tissue