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: 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:
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Authors | Kimihiko Mitsutomi, Takayuki Masaki, Takanobu Shimasaki, Koro Gotoh, Seiichi Chiba, Tetsuya Kakuma, Hirotaka Shibata |
Journal | Metabolism: clinical and experimental
(Metabolism)
Vol. 63
Issue 1
Pg. 69-78
(Jan 2014)
ISSN: 1532-8600 [Electronic] United States |
PMID | 24140095
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2013. |
Chemical References |
- Ion Channels
- Leptin
- Mitochondrial Proteins
- Sweetening Agents
- Triglycerides
- Ucp1 protein, mouse
- Uncoupling Protein 1
- Sucrose
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Topics |
- Adipose Tissue
(drug effects)
- Adipose Tissue, Brown
(metabolism)
- Adipose Tissue, White
(drug effects, metabolism)
- Adiposity
(drug effects)
- Animals
- Diet
- Energy Metabolism
(drug effects)
- Hyperinsulinism
(chemically induced)
- Ion Channels
(blood)
- Leptin
(metabolism)
- Mice
- Mitochondrial Proteins
(blood)
- Obesity
(etiology, metabolism)
- Sucrose
(pharmacology)
- Sweetening Agents
(administration & dosage, pharmacology)
- Triglycerides
(metabolism)
- Uncoupling Protein 1
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