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Bitterness is known to be a major sensory element in the formation of preference and rejection of food and hence may regulate dietary intake [5]. In human bitterness perception, orally expressed bitterness receptors (taste receptor type 2, TAS2Rs, T2Rs) act as a signaling gateway [6]. Among the 25 isoforms of the TAS2Rs genes, TAS2R38 and its encoded protein T2R38 are the most intensively studied factors in bitterness-sensing genetics. Studies have suggested that the diplotype of three genetic variations in TAS2R38, A49P (rs713598, G > C), V262A (rs1726866, T > C) and I296V (rs10246939, T > C), control the activity and expression of the receptor, thereby modifying bitterness sensitivity [6]. Individuals with the PAV haplotype (super taster) are more sensitive to the bitterness of phenylthiocarbamide (PTC) and 6-n-propylthiouracil (PROP); however, those with the AVI haplotype were less sensitive to those compounds (non-taster) [6]. Therefore, the TAS2R38 diplotype was associated with differential intake of cruciferous vegetables, which contain glucosinolates with the thiourea moiety, an agonist of T2R38 [7]. Furthermore, the genetic variation influenced the intake of fruit, sweets, fat and alcohol over bitter-tasting foods [8,9,10,11].

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Results: Following the PRISMA flowchart, finally 103 articles were included in the review. Among the reviewed studies, 43 were rated to have good quality, 47 were rated to have moderate quality, and 13 were rated to have low quality. The majority of the studies assessed the association of genetic variants with the bitter taste modality, followed by articles analyzing the impact of polymorphisms on sweet and fat preferences. The number of studies investigating the association between umami, salty, and sour taste qualities and genetic polymorphisms was limited.

As expected, the majority of studies focused on candidate genes and relevant variants, with TAS2R38 the most extensively studied (n = 40) (Kim et al., 2003; Duffy et al., 2004a; Mennella et al., 2005; Sandell and Breslin, 2006; Sacerdote et al., 2007; Timpson et al., 2007; Hayes et al., 2008; Duffy et al., 2010; Ooi et al., 2010; Wooding et al., 2010; Calò C et al., 2011; Feeney et al., 2011; Gorovic N et al., 2011; Lucock et al., 2011; Mennella et al., 2011a; Cabras et al., 2012; Campbell et al., 2012; Colares-Bento et al., 2012; Negri et al., 2012; Allen et al., 2013a; Behrens et al., 2013; Inoue et al., 2013; Laaksonen et al., 2013; Melis et al., 2013; Allen et al., 2014; Bering et al., 2014; Feeney et al., 2014; Garneau et al., 2014; Keller et al., 2014; Ledda et al., 2014; Mennella et al., 2014a; Robino et al., 2014; Melis et al., 2015; Nolden et al., 2016; Bella et al., 2017; Carrai et al., 2017; Deshaware and Singhal, 2017; Feeney et al., 2017; Risso et al., 2017), followed by TAS2R31 (n = 7) (Pronin et al., 2007; Roudnitzky et al., 2011; Allen et al., 2013a; Allen et al., 2013b; Hayes et al., 2015; Roudnitzky et al., 2015; Nolden et al., 2016), TAS2R19 (n = 6) (1835, Reed et al., 2010; Hayes et al., 2011; Roudnitzky et al., 2015), TAS2R4 (n = 6) (Roudnitzky et al., 2011; Allen et al., 2013a; Allen et al., 2014; Bering et al., 2014; Risso et al., 2017), TAS2R5 (n = 3) (Hayes et al., 2011; Nolden et al., 2016; Carrai et al., 2017), and TAS2R9 (n = 2) (Allen et al., 2013a; Allen et al., 2013b) (Table 1). The association of rs227433 (CA6) with PROP phenotype was inconclusive (Padiglia et al., 2010; Calò C et al., 2011; Cabras et al., 2012; Melis et al., 2013; Bering et al., 2014; Feeney and Hayes, 2014; Risso et al., 2017) (presented in Table 1). The effect of other TAS2R gene polymorphisms were demonstrated by single studies only (presented in Supplementary Table 1). The assessment of perceived bitterness of PROP