Allelic Variation in Taste Genes Is Associated with Taste and Diet Preferences and Dental Caries

Abstract

Taste and diet preferences are complex and influenced by both environmental and host traits while affecting both food selection and associated health outcomes. The present study genotyped 94 single nucleotide polymorphisms (SNPs) in previously reported taste and food intake related genes and assessed associations with taste threshold (TT) and preferred intensity (PT) of sweet, sour and bitter, food preferences, habitual diet intake, and caries status in healthy young Swedish men and women (n = 127). Polymorphisms in the GNAT3, SLC2A4, TAS1R1 and TAS1R2 genes were associated with variation in TT and PT for sweet taste as well as sweet food intake. Increasing PT for sweet was associated with increasing preference and intake of sugary foods. Similarly, increasing TT for sour was associated with increasing intake of sour foods, whereas the associations between food preference/intake and TT/PT for bitter was weak in this study group. Finally, allelic variation in the GNAT3, SLC2A2, SLC2A4, TAS1R1 and TAS1R2 genes was associated with caries status, whereas TT, PT and food preferences were not. It was concluded that variations in taste receptor, glucose transporter and gustducin encoding genes are related to taste perception, food preference and intake as well as the sugar-dependent caries disease.

Oral Microbiota Profile Associates with Sugar Intake and Taste Preference Genes

“…However, non-genetic and non-lifestyle linked factors have also been indicated to influence food habits, i.e., oral microbiota as well as gut microbiota have been suggested to modulate taste perception and eating behaviours [20][21][22][23]. We, and others, have shown that the intake of and preference for sweet foods are associated with polymorphisms in sweet and bitter taste receptor encoding genes, such as TAS1R2, TAS1R3 and TAS2R38, but also glucose transporter genes (SCL2 and SCL4) and the gustducin-encoding (GNAT3) gene [24,25].…”

“…Genotyping of 121 Single Nucleotide Polymorphisms (SNPs) in the TAS1R1, TAS1R2, TAS1R3, TAS2R16, TAS2R38, TAS2R50, SLC2A2, SLC2A4, GNAT3, CA6, SCN1B and TRPV1 taste-associated genes was performed at SciLife, Uppsala as described previously [24]. One SNP marker received a call rate of 0%.…”

Heritability of Oral Microbiota and Immune Responses to Oral Bacteria

“…Understanding the host mechanisms which regulate the oral microbiota composition and function may, therefore, provide novel approaches to treat dental diseases. These mechanisms might involve genetic host regulation of immune response as suggested by the results of the present paper, but also a range of other mechanisms, such as the expression of (glyco) proteins/peptides, which regulate bacteria attachment or metabolism [63] or genetic effects on host behavior such as innate food preferences [15,22,64]. Future studies, including genome-wide host genetic information and oral microbiota data, may help establish these mechanisms.…”

Differences in Sweet Taste Perception and Its Association with the Streptococcus mutans Cariogenic Profile in Preschool Children with Caries

“…Among many factors influencing the increased risk of caries, genetic susceptibility plays an important role, increasing the appearance of the problem by about 50% [86][87][88]. Having a genetic background predisposition to prefer a particular taste may be related to the preference or rejection of certain foods by children.…”

“…Having a genetic background predisposition to prefer a particular taste may be related to the preference or rejection of certain foods by children. In particular, genes ( gnat3 , slc2a4 , tas1r1 , and tas1r2 ) related to the sweet taste receptor, glucose transport (GLUT2), or specific clinical genotypes, have a decisive influence on the development of specific preferences regarding taste [ 88 ]. Systematic reviews show that, despite educational programs or interventions concerning nutritional behavior among children, the problem still exists [ 89 , 90 , 91 , 92 ].…”