Differential effects of sucrose and fructose on dietary obesity in four mouse strains

PHYSIOLOGY & BEHAVIOR

卷:101

Article

Glendinning, John I.¹  Breinager, Lindsey¹  Kyrillou, Emily¹  Lacuna, Kristine¹  Rocha, Rotsen¹  Sclafani, Anthony² 

[1] Columbia Univ Barnard Coll, Dept Biol Sci, New York, NY 10027 USA

[2] CUNY Brooklyn Coll, Dept Psychol, Brooklyn, NY 11210 USA

关键词: Sugar-induced obesity;    Hyperphagia;    Mice;    Sweet taste;    Sucrose;    Fructose;   

DOI  :  10.1016/j.physbeh.2010.06.003

来源: Elsevier

【 摘 要 】

We examined sugar-induced obesity in mouse strains polymorphic for Tas1r3, a gene that codes for the T1R3 sugar taste receptor. The T1R3 receptor in the FVB and B6 strains has a higher affinity for sugars than that in the AKR and 129P3 strains. In Experiment 1. mice had 40 days of access to lab chow plus water, sucrose (10 or 34%), or fructose (10 or 34%) solutions. The strains consumed more of the sucrose than isocaloric fructose solutions. The pattern of strain differences in caloric intake from the 10% sugar solutions was FVB>129P3 = B6>AKR: and that from the 34% sugar solutions was FVB>129P3>B6 >= AKR. Despite consuming more sugar calories, the FVB mice resisted obesity altogether. The AKR and 129P3 mice became obese exclusively on the 34% sucrose diet, while the 86 mice did so on the 34% sucrose and 34% fructose diets. In Experiment 2, we compared total caloric intake from diets containing chow versus chow plus 34% sucrose. All strains consumed between 11 and 25% more calories from the sucrose-supplemented diet. In Experiment 3, we compared the oral acceptability of the sucrose and fructose solutions, using lick tests. All strains licked more avidly for the 10% sucrose solutions. The results indicate that in mice (a) Tas1r3 genotype does not predict sugar-induced hyperphagia or obesity; (b) sucrose solutions stimulate higher daily intakes than isocaloric fructose solutions; and (c) susceptibility to sugar-induced obesity varies with strain, sugar concentration and sugar type. (C) 2010 Elsevier Inc. All rights reserved.

【 授权许可】

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