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Endocrine Abstracts (2021) 73 AEP876 | DOI: 10.1530/endoabs.73.AEP876

ECE2021 Audio Eposter Presentations Late Breaking (114 abstracts)

Influence of bitter taste gene TAS2R38 on endocrinometabolic and anthropometric parameters in a sample with thyroid disease

Marta Mendes Costa1, Ana Carolina Santos2, 3, Joana Ferreira2, 3, Mário Rui Mascarenhas2, 4, Manuel Bicho2, 5, Ana Paula Barbosa4, 5, 7 & Alda Pereira da Silva6, 8, 9

1Faculty of Medicine, University of Lisbon, Lisbon, Portugal; 2Genetic Laboratory and Ecogenetic and Human Health Group, Environmental Health Institute- ISAMB, Faculty of Medicine, University of Lisbon, Lisbon, Portugal; 3Institute of Scientific Investigation Bento da Rocha Cabral, Lisbon, Lisbon, Portugal; 4Endocrinology, Metabolism and Diabetes Clinic of Lisbon, Lisbon, Portugal; 5Institute of Scientific Investigation Bento da Rocha Cabral, Lisbon, Portugal; 6Genetic Laboratory and Ecogenetic and Human Health Group, Environmental Health Institute- ISAMB, Faculty of Medicine, University of Lisbon;, Lisbon, Portugal; 7Endocrinology, Diabetes and Metabolism Service, Santa Maria, North Lisbon Universitary Hospital Centre, Lisbon, Portugal; 8University Clinic of General Practice, Faculty of Medicine, Lisbon University, Lisbon, Portugal; 9Institute of Preventive Medicine and Public Health, Environmental Health Institute– ISAMB, Faculty of Medicine, University of Lisbon, Lisbon, Portugal

Background and objectives

TAS2R38 is a bitter taste gene that can influence food consumption depending on its single nucleotide polymorphisms (SNPs) leading to aminoacid substitutions in the receptor protein P49A (proline/alanine), A262V (alanine/valine) e V296I (valine/isoleucine). Subjects with at least one PAV (proline-alanine-valine) copy are bitter tasters, while AVI homozygotes are non-tasters. Other variants have intermediate bitter tasting: AAV<AAI<PAI. TAS2R38 is expressed in thyroid and other organs. This study evaluates TAS2R38 gene polymorphisms influence in thyroid function, metabolism and body composition.


DNA of 167 individuals (79% female) 24.6% eutrophic, 43.7% overweight and 31.7% obese was genotyped by endpoint analysis. From these, 79 had thyroid functional disease (hypothyroidism n = 41) compared with 88 controls. Anthropometric parameters BMI (kg/m2), fat mass (%), total fat mass (kg), total lean mass (kg) determined by DEXA; metabolic/hormonal parameters by standard methods: triglyceridaemia (mg/dl), HDL (mg/dl), LDL (mg/dl), glycaemia (mg/dl), TSH (mcUI/ml), T3 (ng/dl), T4 (ng/dl), FT4 (ng/dl). Leptin (ng/ml) by ELISA. Statistics: χ2 and ANOVA, significance for P <0.05.


There were differences (p<0.001) in the distribution of diplotypes between subgroups being respectively for hypothyroidism-hyperthyroidism-controls (%): PVV/AVI (65.4; 64.3; 0); AVV/AVV (19.2; 10.7; 0); PVI/PVI (7.7; 7.1; 31.6); PVV/AVV (3.8; 7.1; 0); AAV/AAV (3.8; 0; 15.8); PVV/AAI (0; 0; 46.1); PVV/PAI (0; 0; 5.3); AVV/AVI (0; 3.6; 0); PAV/AAV (0; 0; 1.3); PVV/PV (0; 7.1;0). Diplotypes were associated with fat mass (P = 0.025); leptin (P = 0.019) and triglyceridaemia (P = 0.048). For PVV/AVI and PVV/AAI diplotypes, average values were respectively: fat mass 37.45±6.67 and 34.45±7; leptin: 56.80±37.32 and 50.85±54.16; triglyceridaemia: 99.64±49.76 and 94.52±55.97. Significant association between the SNP A262V and hyper/hypothyroidism (P <0.001); total lean mass (P = 0.012) and fat mass (P = 0.03), triglyceridaemia (P = 0.05) and TSH (P = 0.025). The SNP V296I was associated with total lean mass (P = 0.014). Metabolic and anthropometric variables associated with hyper/hypothyroidism: total fat mass (P = 0.02); BMI (P = 0.002), glycaemia (P = 0.035), triglyceridaemia (P = 0.05), TSH (P = 0.008), FT4 (P = 0.027). No significant differences for other parameters.


The distribution of TAS2R38 diplotypes differed between the control and hyperthyroidism or hypothyroidism samples. The haplotype AVI (SNP A262V) associated with metabolic and body composition parameters and with less bitter sensitivity may be a clue for dysfunctional thyroid. This could be due to exogenous factors such as higher ingestion of bitter goitrogenic compounds inducing hypothyroidism or, on the other hand, predisposition to hyperthyroidism via higher resistance to antithyroid effects of unknown endogenous factors in individuals with the AVI variant. In conclusion, TAS2R38 gene influences thyroid function witch modulates metabolism and body composition.

Volume 73

European Congress of Endocrinology 2021

22 May 2021 - 26 May 2021

European Society of Endocrinology 

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