Consumption of a sugar-sweetened soft drink in combination with a Western-type diet alters taste markers independent of body weight development
Thu-P1-059
Presented by: Barbara Lieder
Taste dysfunction has been reported for obese individuals in mice and men, but more recent studies indicated that certain dietary stimuli also lead to taste deficits in mice without the onset of obesity. Here we investigated whether the long-term intake of a typical caffeinated sugar-sweetened soft drink (SSB) alters markers for taste function when applied in combination with a standard chow (STD) or a Western-type Diet (WD).
Adult male CD1 mice had ad libitum access to tap water or SSB in combination with either STD (n=10-12) or a WD (commercial cheeseburgers, n=7-8) for 24 weeks. Energy intake from fluid and food was monitored three times a week. Body weight and composition, waist circumference, glucose and lipid profile, and blood pressure were analyzed at the end of the intervention. The number and size of the fungiform papillae for calculation of the chemosensory surface at the tip of each tongue was examined after staining of the tongue with brilliant blue and mRNA levels of genes associated with the different cell types of taste buds and taste receptors were analyzed in the circumvallate papillae (CV) using a cDNA microarray and qPCR.
Although the overall energy intake was higher in the WD groups, there was no difference in body weight and composition, in the blood lipids, and markers for glucose intolerance between the SSB and water groups at the end of the experiment. The total chemosensory surface from the fungiform papillae was reduced after SSB compared to water intake in the WD group by 36 ± 19 % (p<0.05). Transcriptome analysis of the CV revealed an upregulation of marker genes for basal taste bud cells, of GLUT-1, and several bitter taste receptors targeted by caffeine and in the SSB group fed a WD.
In conclusion, the study supports an interplay of sugar, high-nutrient diets, and chemosensory function on a molecular level independent of body weight development in mice, which could influence food selection.
Adult male CD1 mice had ad libitum access to tap water or SSB in combination with either STD (n=10-12) or a WD (commercial cheeseburgers, n=7-8) for 24 weeks. Energy intake from fluid and food was monitored three times a week. Body weight and composition, waist circumference, glucose and lipid profile, and blood pressure were analyzed at the end of the intervention. The number and size of the fungiform papillae for calculation of the chemosensory surface at the tip of each tongue was examined after staining of the tongue with brilliant blue and mRNA levels of genes associated with the different cell types of taste buds and taste receptors were analyzed in the circumvallate papillae (CV) using a cDNA microarray and qPCR.
Although the overall energy intake was higher in the WD groups, there was no difference in body weight and composition, in the blood lipids, and markers for glucose intolerance between the SSB and water groups at the end of the experiment. The total chemosensory surface from the fungiform papillae was reduced after SSB compared to water intake in the WD group by 36 ± 19 % (p<0.05). Transcriptome analysis of the CV revealed an upregulation of marker genes for basal taste bud cells, of GLUT-1, and several bitter taste receptors targeted by caffeine and in the SSB group fed a WD.
In conclusion, the study supports an interplay of sugar, high-nutrient diets, and chemosensory function on a molecular level independent of body weight development in mice, which could influence food selection.