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, PTC, quinine, caffeine/coffee, unsweetened grapefruit juice, berry juice samples and extracts, salad rocket, stevioside, thioamide, aloin, salicin, saccharin, methimazole, acesulfame potassium, denatonium benzoate, absinthin, amarogentin, cascarillin, grosheimin, quassin, capsaicin, piperine, gentiobiose, aspartame, rebaudioside A and D, alcohol/wine, and preference for bitter tasting foods and beverages (broccoli, artichoke, chicory, glucosinolate-generating vegetables, coffee, dark chocolate) were applied as phenotyping methods. Publications on consumption of bitter foods and drinks (Brassica/cruciferous vegetables, coffee; measured by the food frequency questionnaire, 24-h dietary recall, and the 3-day food record) only appeared among the search results and were considered for further evaluation as preference, if it was supported by background information, that the consumption was based on free choice and not influenced by other factors.
Much less is known about the effect of the genetic alterations of other taste 2 receptors (TAS2Rs), which proteins also function as bitter taste receptors. Respondents for TAS2R31 receptors (formerly TAS2R44) are compounds with no common chemical substructure (acesulfame K, famotidine, diphenidol) (Meyerhof et al., 2009). Research included in our review (n = 7) focused on two polymorphisms rs10845293 (Ala227Val) and rs10772423 (Val240Ile) located in this gene (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). The Val240Ile SNP was associated with the bitter compounds amarogentin [found in gentian (Gentiana lutea) or in Swertia chirata] (Keil et al., 2000) and grosheimin [present in artichokes (Cravotto et al., 2005)] intensities, detection and recognition threshold, quinine bitterness and grapefruit liking. Moreover, Val240 homozygotes reported less bitterness from the artificial sweetener acesulfame potassium than the Ile240 homozygotes (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). This latter finding is in accordance with in vitro study results, whereas acesulfame K activated TAS2R43 and TAS2R44 at concentrations known to stimulate bitter taste (Kuhn et al., 2004). The same polymorphism showed no association with bitterness of capsaicin, piperine, and ethanol (Nolden et al., 2016). The bitterness perception from capsaicin and piperine is characterized by individual diversities (Green and Hayes, 2004) and the sensitivity to perceived bitterness of alcohol correlates with PROP phenotypes (Lanier et al., 2005), but based on findings of these studies it was not related to TAS2R31 genetic variants (Nolden et al., 2016).
Moreover, several studies in human nutrition have suggested that the PROP phenotype may serve as a general marker for oral sensations and food preferences, and influence dietary behavior and nutritional status (Tepper, 2008). Given the nutritional importance of dietary lipids and sugars an extensive research has investigated the impact of PROP taster status on sweet and fat consumption. Most studies focusing on the relationship between taster status and dietary fat perception (Tepper and Nurse, 1997; Kirkmeyer and Tepper, 2003; Duffy et al., 2004b; Prescott et al., 2004; Hayes and Duffy, 2007; Hayes and Duffy, 2008), but not all (Drewnowski et al., 1998b; Drewnowski et al., 2007) reported that taster individuals had a lower ability to distinguish fat content and creaminess in certain fatty foods and gave higher taste intensity ratings for linoleic acid, than non-tasters (Ebba et al., 2012). Moreover, PROP non-tasters possessed preferences for dietary fat (Forrai and Bánkövi, 1994; Tepper and Nurse, 1998; Duffy, 2000; Keller et al., 2002; Hayes and Duffy, 2007) and consumed more servings of discretionary fats and high-energy foods per day compared to tasters (Keller et al., 2002; Tepper et al., 2011). Findings to elucidate the association between PROP taster status and sweet preference and sugar intake were inconclusive. Some studies found that more sensitive individuals to PROP showed lower sweet preference (Looy et al., 1992; Duffy, 2000; Hayes and Duffy, 2007; Yeomans et al., 2007). Other investigators found that sucrose tasted sweeter to tasters (Gent and Bartoshuk, 1983), but some found no link between PROP taster status and hedonic ratings for sweet (Gent and Bartoshuk, 1983; Drewnowski et al., 1997; Drewnowski et al., 2007; Von Atzingen and Silva, 2012) and the consumption sweet beverages (Wijtzes et al., 2017). Accordingly the role of bitter-taster status in shaping dietary preferences is certainly not negligible, but more research is needed to determine its effect on nutrition, besides the intake of bitter-tasting foods. Although the focus of this review was on genetic variants affecting taste, studies examining associations with PROP/PTC were not included despite their strong linkage with TAS2R38 genotype. This may have resulted in some relevant papers not being included in the analyses and discussion.
The signal transduction of sweet taste is linked to heterodimers of two G protein-coupled receptors T1R2 and T1R3) (Pronin et al., 2007; Roudnitzky et al., 2015), which are encoded by genes clustered on chromosome 1 (Liao and Schultz, 2003). TAS1R2 is characterized by an increased level of genetic diversity, furthermore TAS1R3 is more conserved (Kim et al., 2006). Candidate gene studies of sweet preference targeted the polymorphic sites located in T1R2 and T1R3 genes involved in the signal transduction of this taste modality (Fushan et al., 2009; Eny et al., 2010; Mennella et al., 2014b; Dias et al., 2015; Joseph et al., 2016; Han et al., 2017), with results not allowing further conclusions to make, since only the effect of the functional Ile191Val (rs35874116) variation (Dias et al., 2015) and the intronic rs3935570 yielded positive findings (Eny et al., 2010; Han et al., 2017) (Table 2). The most convincing results were related to variants in the bitter taste receptor gene (TAS2R38). These polymorphisms were reported to affect the sensory experience of sweet taste, changes in taste sensitivity and preference, and sweet food intake (Lipchock et al., 2012; Suomela et al., 2012; Keller et al., 2014; Sandell et al., 2014; Joseph et al., 2016; Pawellek et al., 2016; Perna et al., 2018) (Table 2), with the only exclusion a study by Ooi et al. (2010). The genetically-determined taster phenotype preferred higher sucrose concentrations (Lipchock et al., 2012), had lower detection thresholds (Joseph et al., 2016), and consumed more sweet tasting foods (Suomela et al., 2012; Keller et al., 2014; Sandell et al., 2014; Pawellek et al., 2016; Perna et al., 2018) whereas genetically determined non-taster individuals did not prefer sweet foods (Ooi et al., 2010), despite that the PROP phenotype without underlying genetic investigations showed inconclusive findings with sugar preference and intake in adults (Gent and Bartoshuk, 1983; Looy et al., 1992; Drewnowski et al., 1998b; Drewnowski et al., 1997; Duffy, 2000; Hayes and Duffy, 2007; Yeomans et al., 2007; Von Atzingen and Silva, 2012; Wijtzes et al., 2017), which is probably related to other genetic variants that influence bitter perception, and also in children that may be explained by age-related changes in taste perception and preference, beyond genetic factors (reviewed in Keller and Adise, 2016).
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