Taste preferences and obesity

Abstract

Introduction: Genetically determined violation of taste preferences leads to inversion of taste perception and overeating, distorting the homeostatic feedback of the peripheral energy status with hedonic centers, causing obesity. According to previous research the gene TAS2R38 (taste 2 receptor member 38) has the greatest contribution to the development of metabolically unhealthy obesity (MUO). Aim of the study was to study the role of the single nucleotide variant (SNV) gene TAS2R38 in the development of MUO in children. Material and methods: 205 obese children 6-18 years old were examined by clinical and laboratory methods, including anthropometric, immunobiochemical, and psychological, using the Food and Beverage Preference Questionnaire (FBPQ) and next-generation sequencing. The main group ( n = 124) consisted of children with MUO, according to the recommendations of the expert group of the IDEFICS, 2014. The control group ( n = 81) consisted of children with metabolically healthy obesity. The following statistical methods were used: analysis of variance, odds ratio, Spearman’s correlation analysis, Wald’s sequential analysis. Results: The level of the mean preference for bitter food in the main group was 2.75 ±0.15 points, while in the control group it was 3.24 ±0.14 points; Student’s test, t = 2.39, p < 0.02. The analysis of food diaries in children showed a positive correlation between the daily rejection of fresh vegetables and the development of MUO ( p = 0.32) with a prognostic coefficient of 2.7; p < 0.05. Three SNVs of the TAS2R38 gene (missense muta-tions) were diagnosed. The probability of detecting the heterozygous C/G variant of the rs713598 genotype of TAS2R38 in the main group was 1.75 times higher than in the control group ( p < 0.05). Conclusions: Low taste preferences for bitter foods are associated with the development of MUO in children. rs713598 (C/G) has the greatest association with the development of metabolically unhealthy obesity among the SNVs of the TAS2R38 gene we have identified.