Genetic variations of the bitter taste receptor TAS2R38 are associated with obesity and impact on single immune traits. Issue 7 (27th May 2016)

• Record Type: Journal Article
• Authors: Ortega, Francisco J.; Agüera, Zaida; Sabater, Mònica; Moreno‐Navarrete, José M; Alonso‐Ledesma, Isabel; Xifra, Gemma; Botas, Patricia; Delgado, Elías; Jimenez‐Murcia, Susana; Fernández‐García, José C.; Tinahones, Francisco J; Baños, Rosa M.; Botella, Cristina; de la Torre, Rafael; Frühbeck, Gema; Rodrigüez, Amaia; Estivill, Xavier; Casanueva, Felipe; Ricart, Wifredo; Fernández‐Aranda, Fernando; Fernández‐Real, José M.
• Is Part Of: Molecular nutrition & food research. Volume 60:Issue 7(2016)
• Page Start: 1673
• Page End: 1683
• Publication Date: 2016-05-27
• Subjects: Haplotypes -- Immune system -- Mannose‐binding lectin -- Metabolism -- Obesity -- Surfactant protein D -- Taste receptor type 2 member 38; Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201500804
• Languages: English
• ISSNs: 1613-4125

Abstract

Abstract : Here, we demonstrate that genetic variations that underlie functionality of the TAS2R38, a receptor that regulates the ability to identify bitter‐tasting compounds, may impact on phenotypic and clinical outputs affecting extreme weight conditions (i.e., obesity and anorexia nervosa), being also associated with proteins partaking in innate immunity (i.e., surfactant protein D (SPD) and mannanbinding lectin (MBL)). Abstract : Scope: Changes in genetic variations affecting the taste receptor, type 2, member 38 (TAS2R38) may identify the interacting mechanism leading to obesity and potential associations with proteins partaking in innate immunity, such as surfactant protein D (SPD) and mannan‐binding lectin (MBL). Methods and results: We evaluated haplotypes of the bitter‐taste receptor TAS2R38 in an identification sample of 210 women in different weight conditions, including anorexia nervosa and obesity. The association with SPD and MBL was tested in an independent sample picturing general population ( n = 534). The relationship with obesity was validated in an extended final sample of 1319 participants. In the sample comprised of women in extreme weight conditions, increased obesity was identified in AVI/AVI subjects (OR = 2.5 [1.06–6.11], p = 0.035). In the sample picturing general population, increased SPD and MBL concentrations were found in nonsmoking AVI carriers. In this cohort, smoking and obesity blunted associations between TAS2R38 haplotypes and SPD and MBL. In the extended sample, the association of AVI/AVI haplotypes with increased obesity was also identified (OR = 1.4 [0.99/1.85], p = 0.049), being more robust in subjects aged <40 years (OR = 1.9 [1.06/3.42], p = 0.031). Conclusion: Current data reinforce the impact of TAS2R38 gene on phenotypic and clinical outputs affecting obesity, showing significant associations with extreme weight conditions (i.e., obesity and anorexia nervosa), and changes in both olfactory capacity and immune traits.