The role of the Sac locus in the alcohol taste preference in inbred mouse strains

Муровец, В. О.; Золотарев, В. А.; Bachmanov, Alexander A.

doi:10.1134/s001249661003004x

Cited by 4 publications

(2 citation statements)

References 16 publications

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“…This suggests that the Tas1r3 gene is identical to the Ap3q locus. Consistent with this, allelic variation of the Tas1r3 gene in congenic and knockout mice has pleiotropic effects on ingestive responses to sweeteners and ethanol in the long‐term and brief‐access tests, and influences taste quality perception of ethanol . These data suggest that Tas1r3 alleles influence perception of the sweet taste component of ethanol flavour.…”

Section: Sweet Taste Preferences and Alcohol Intakesupporting

confidence: 64%

Genetics of sweet taste preferences

Bachmanov

Bosak

Floriano

et al. 2011

Flavour & Fragrance J

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Sweet taste is a powerful factor influencing food acceptance. There is considerable variation in sweet taste perception and preferences within and among species. Although learning and homeostatic mechanisms contribute to this variation in sweet taste, much of it is genetically determined. Recent studies have shown that variation in the T1R genes contributes to within- and between-species differences in sweet taste. In addition, our ongoing studies using the mouse model demonstrate that a significant portion of variation in sweetener preferences depends on genes that are not involved in peripheral taste processing. These genes are likely involved in central mechanisms of sweet taste processing, reward and/or motivation. Genetic variation in sweet taste not only influences food choice and intake, but is also associated with proclivity to drink alcohol. Both peripheral and central mechanisms of sweet taste underlie correlation between sweet-liking and alcohol consumption in animal models and humans. All these data illustrate complex genetics of sweet taste preferences and its impact on human nutrition and health. Identification of genes responsible for within- and between-species variation in sweet taste can provide tools to better control food acceptance in humans and other animals.

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Section: Sweet Taste Preferences and Alcohol Intakesupporting

confidence: 64%

Genetics of sweet taste preferences

Bachmanov

Bosak

Floriano

et al. 2011

Flavour & Fragrance J

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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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