title: Differential effects of sucrose and fructose on dietary obesity in four mouse strains.
abstract: 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 40days 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 B6 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.
authors.affiliation: Department of Biological Sciences, Barnard College, Columbia University, New York, NY 10027, United States. jglendinning@barnard.edu
authors.forename: John I
authors.initials: JI
authors.lastname: Glendinning
authors.forename: Lindsey
authors.initials: L
authors.lastname: Breinager
authors.forename: Emily
authors.initials: E
authors.lastname: Kyrillou
authors.forename: Kristine
authors.initials: K
authors.lastname: Lacuna
authors.forename: Rotsen
authors.initials: R
authors.lastname: Rocha
authors.forename: Anthony
authors.initials: A
authors.lastname: Sclafani
mesh_terms: D000284:Administration, Oral; D000704:Analysis of Variance; D000818:Animals; D004305:Dose-Response Relationship, Drug; D004435:Eating / Q000187:drug effects / Q000235:genetics; D002149:Energy Intake / Q000235:genetics* / Q000502:physiology; D005260:Female; D005518:Food Preferences / Q000502:physiology; D005632:Fructose / Q000008:administration & dosage / Q000378:metabolism; D006963:Hyperphagia / Q000139:chemically induced* / Q000378:metabolism; D008297:Male; D051379:Mice; D057507:Mice, 129 Strain; D008806:Mice, Inbred AKR; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000235:genetics* / Q000378:metabolism; D011897:Random Allocation; D043562:Receptors, G-Protein-Coupled / Q000235:genetics* / Q000502:physiology; D013045:Species Specificity; D013395:Sucrose / Q000008:administration & dosage / Q000378:metabolism; D013649:Taste / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D055697:Taste Perception / Q000235:genetics; D013997:Time Factors; D015430:Weight Gain / Q000187:drug effects / Q000235:genetics / Q000502:physiology
chemical_list: D043562:Receptors, G-Protein-Coupled; C431926:taste receptors, type 1; D005632:Fructose; D013395:Sucrose