Genetics of sweet taste preferences

Bachmanov, Alexander A.; Bosak, Natalia P.; Floriano, Wely B.; Inoue, Masato; Li, Xia; Lin, Cailu; Муровец, В. О.; Reed, Danielle R.; Золотарев, В. А.; Beauchamp, Gary K.

doi:10.1002/ffj.2074

Cited by 76 publications

(43 citation statements)

References 181 publications

(220 reference statements)

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“…This may not be case with other inbred mouse strains, however, given the strain differences in sweetener preferences [1] as well as in sugar-conditioned preferences [30]. The present experiment investigated this possibility by comparing flavor conditioning by SS and fructose in FVB and CAST strains.…”

Section: Experiments 7 Fructose and Sucralose + Saccharin Conditiomentioning

confidence: 97%

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Flavor preferences conditioned by nutritive and non-nutritive sweeteners in mice

Sclafani

Ackroff

2017

Physiology & Behavior

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Recent studies suggest that preferences are conditioned by nutritive (sucrose) but not by non-nutritive (sucralose) sweeteners in mice. Here we compared the effectiveness of nutritive and non-nutritive sweeteners to condition flavor preferences in three mouse strains. Isopreferred sucrose and sucralose solutions both conditioned flavor preferences in C57BL/6J (B6) mice but sucrose was more effective, consistent with its post-oral appetition action. Subsequent experiments compared flavor conditioning by fructose, which has no post-oral appetition effect in B6 mice, and a sucralose + saccharin mixture (SS) which is highly preferred to fructose in 24-h choice tests. Both sweeteners conditioned flavor preferences but fructose induced stronger preferences than SS. Training B6 mice to drink a flavored SS solution paired with intragastric fructose infusions did not enhance the SS-conditioned preference. Thus, the post-oral nutritive actions of fructose do not explain the sugar’s stronger preference conditioning effect. Training B6 mice to drink a flavored fructose solution containing SS did not reduce the sugar-conditioned preference, indicating that SS does not have an off-taste that attenuates conditioning. Although B6 mice strongly preferred flavored SS to flavored fructose in a direct choice test, they preferred the fructose-paired flavor to the SS-paired flavor when these were presented in water. Fructose conditioned a stronger flavor preference than an isopreferred saccharin solution, indicating that sucralose is not responsible for the limited SS conditioning actions. SS is highly preferred by FVB/NJ and CAST/EiJ inbred mice, yet conditioned only weak flavor preferences. It is unclear why highly or equally preferred non-nutritive sweeteners condition weaker preferences than fructose, when all stimulate the same T1r2/T1r3 sweet receptor. Recent findings support the existence of non-T1r2/T1r3 glucose taste sensors; however, there is no evidence for receptors that respond to fructose but not to non-nutritive sweeteners.

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Section: Experiments 7 Fructose and Sucralose + Saccharin Conditiomentioning

confidence: 97%

“…Alternatively, rats and mice may differ in their ability to acquire sweet taste-based preferences. Also given inbred strain differences in sweetener preferences and flavor conditioning [1,30], some mouse strains may be more susceptible than others to flavor conditioning by sweet taste.…”

Section: Introductionmentioning

confidence: 99%

Flavor preferences conditioned by nutritive and non-nutritive sweeteners in mice

Sclafani

Ackroff

2017

Physiology & Behavior

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“…Children with a family history of alcoholism also prefer a higher sucrose concentration compared to children without a family history of alcoholism; however, this was only the case for children who were also experiencing depressive symptomatology [83]. Variation in the taste receptor type one family of genes ( TAS1R1 , TAS1R2, and TAS1R3 ) influences sweet liking [84] and there is a linkage peak (LOD = 3.5) on chromosome 16 at 16p11.2 (marker D16S753) for frequency of sweet food consumption [80]. However, whether variation in the TAS1 genes and other sweet-liking genomic regions are associated with AUD has not been systematically examined, representing an important direction for future research.…”

Section: Promising Potential Endophenotypesmentioning

confidence: 99%

“…Animal models have also provided some validation of sweet liking as a strong candidate endophenotype for AUD and for addiction phenotypes more broadly [106, 84]. Rats selected for high saccharin intake consumed more ethanol relative to rats selected for low saccharin intake [107], and they exhibit greater ethanol withdrawal [108].…”

Section: Aud Endophenotypes In Animal Modelsmentioning

confidence: 99%

Endophenotypes for Alcohol Use Disorder: An Update on the Field

2015

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The endophenotype concept was first proposed as a strategy to use (purportedly) genetically simpler phenotypes in gene identification studies for psychiatric disorders, and is distinct from the closely related concept of intermediate phenotypes. In the area of alcohol use disorder (AUD) research, two candidate endophenotypes have produced replicable genetic associations: level of response to alcohol and neurophysiology markers (e.g., event-related oscillations and event-related potentials). Additional candidate endophenotypes from the cognitive, sensory, and neuroimaging literatures show promise, although more evidence is needed to fully evaluate their potential utility. Translational approaches to AUD endophenotypes have helped characterize the underlying neurobiology and genetics of AUD endophenotypes and identified relevant pharmacological interventions. Future research that capitalizes on the polygenic nature of endophenotypes and emphasizes endophenotypes that may change across development will enhance the usefulness of this concept to understand the genetically-influenced pathways toward AUD.

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“…The receptor involved in the perception of sweet taste of carbohydrates, certain amino acids, and non-caloric sugar substitutes represents a heterodimer that is composed of two transmembrane protein subunits, T1R2 and T1R3, encoded by the Tas1r2 and Tas1r3 genes [11, 12]. Polymorphism of the Tas1r3 has been shown to underlie the among-strain differences in the extent of taste preference for sweet substances, amino acids, and ethanol in mice [13, 14] and among-population differences in that for sucrose and sodium glutamate in humans [12, 15]. Study on the Tas-1 genes in different taxonomic groups of vertebrates allowed explaining many species-specific dietary preferences from the standpoint of physiological genetics.…”

Section: Introductionmentioning

confidence: 99%

The involvement of the T1R3 receptor protein in the control of glucose metabolism in mice at different levels of glycemia

Муровец

Bachmanov

Travnikov

et al. 2014

J Evol Biochem Phys

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The heterodimeric protein T1R2/T1R3 is a chemoreceptor mediating taste perception of sugars, several amino acids, and non-caloric sweeteners in humans and many other vertebrate species. The T1R2 and T1R3 proteins are expressed not only in the oral cavity, but also in the intestine, pancreas, liver, adipose tissue, and in structures of the central nervous system, which suggests their involvement in functions other than gustatory perception. In this study, we analyzed the role of the T1R3 protein in regulation of glucose metabolism in experiments with the gene-knockout mouse strain C57BL/6J–Tas1r3tm1Rfm (Tas1r3−/−), with a deletion of the Tas1r3 gene encoding T1R3, and the control strain C57BL/6ByJ with the intact gene. Glucose tolerance was measured in euglycemic or food-deprived mice after intraperitoneal or intragastric glucose administration. We have shown that in the Tas1r3−/− strain, in addition to the disappearance of taste preference for sucrose, glucose tolerance is also substantially reduced, and insulin resistance is observed. The effect of the Tas1r3 gene knockout on glucose utilization was more pronounced in the euglycemic state than after food deprivation. The baseline glucose level after food deprivation was lower in the Tas1r3−/− strain than in the control strain, which suggests that T1R3 is involved in regulation of endogenous glucose production. These data suggest that the T1R3-mediated glucoreception interacts with the KATP-dependent mechanisms of regulation of the glucose metabolism, and that the main role is likely played by T1R3 expressed in the pancreas and possibly in the central nervous system, but not in the intestinal mucosa, as it was suggested earlier.

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Genetics of sweet taste preferences

Cited by 76 publications

References 181 publications

Flavor preferences conditioned by nutritive and non-nutritive sweeteners in mice

Flavor preferences conditioned by nutritive and non-nutritive sweeteners in mice

Endophenotypes for Alcohol Use Disorder: An Update on the Field

The involvement of the T1R3 receptor protein in the control of glucose metabolism in mice at different levels of glycemia

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