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Clincal Science| Volume 63, ISSUE 1, P69-78, January 2014

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Effects of a nonnutritive sweetener on body adiposity and energy metabolism in mice with diet-induced obesity

Published:October 21, 2013DOI:https://doi.org/10.1016/j.metabol.2013.09.002

      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.

      Abbreviations:

      NNS (nonnutritive sweetener), DIO (diet-induced obesity), BAT (brown adipose tissue), WAT (white adipose tissue), UCP (uncoupling protein), MSL (skeletal muscle), TG (triglyceride), PPAR (peroxisome proliferator-activated receptor), PGC-1 (peroxisome proliferator-activated receptor γ coactivator 1), CPT-1 (carnitine palmitoyltransferase 1), FAS (fatty acid synthetase), POMC (proopiomelanocortin), NPY (neuropeptide Y)

      Keywords

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