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Foroud, Tatiana; Bice, Paula J.; Castelluccio, Peter; Bo, Ronghai; Ritchotte, Aimee; Stewart, Robert B.; Lumeng, Lawrence; Li, T. K.; Carr, Lucinda G.

doi:10.1023/a:1014459912935

Cited by 20 publications

(4 citation statements)

References 33 publications

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“…This association has been observed previously in lines of rats and mice selectively bred for differences in alcohol intake (Stewart et al 1994; Grahame et al 1999; Kampov-Polevoy et al 1999; Foroud et al 2002; Tampier and Quintanilla 2005). On the other hand, additional studies suggest that genetic differences in alcohol drinking in animals (Agabio et al 2000) or differences in family history of alcoholism in humans (Kranzler et al 2001; Tremblay et al 2009) do not always predict differences in sweet preference.…”

Section: Discussionsupporting

confidence: 82%

Derivation and Characterization of Replicate High- and Low-Alcohol Preferring Lines of Mice and a High-Drinking Crossed HAP Line

et al. 2010

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Selectively breeding lines of mice and rats to differ in alcohol intake has proven useful for defining which traits correlate with high alcohol drinking behavior, as well as for creating animal models of alcoholism. This study reports the derivation of two novel sets of selected lines, High Alcohol Preferring (HAP) and Low Alcohol Preferring (LAP) replicate 2 and 3 lines. Mice were mass-selected using the same procedure as in the replicate 1 lines: using HS/Ibg as a progenitor, mice were selected for differences in 2-bottle choice intake of 10% alcohol during a 4-week testing period. In addition, another high drinking line, the crossed HAP (cHAP) line was selectively bred from a progenitors that were a cross of replicate 1 (S27) X replicate 2 (S21) HAP lines. All lines were characterized for saccharin intake. Overall, the response to selection of the HAP and LAP replicate 2 and 3 lines was quite similar. As anticipated, following selection, the cHAP line drank more than either parent HAP line (consuming 26.0 g/kg per day of alcohol by S11), suggesting that this method of crossing replicate lines and selecting from that cross captures more alleles than any single selected line, as well as producing a line with exceptionally high voluntary alcohol intake. As expected, saccharin consumption was highly associated with alcohol consumption; data from all 8 lines (HAP 1, 2, and 3, LAP 1, 2, and 3, HS/Ibg, and cHAP) indicated a genetic correlation between 10% alcohol and 0.32% saccharin intake of 0.917. Overall, these findings show the practicality of developing replicate lines divergent in alcohol preference, and validate a novel procedure for generating very high-drinking mouse populations.

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Section: Discussionsupporting

confidence: 82%

Derivation and Characterization of Replicate High- and Low-Alcohol Preferring Lines of Mice and a High-Drinking Crossed HAP Line

et al. 2010

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“…We have found [20] that strain and individual differences among rats' responses to sweeteners are not related to genotypic variation of the rat Tas1r3 ortholog. Although we cannot eliminate other T1Rs as being involved, the mapping work of other investigators [21] is not consistent with the conclusion that these genes are involved.…”

contrasting

confidence: 75%

Genetics of sweet taste preferences

Bachmanov

Reed

et al. 2002

Pure and Applied Chemistry

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Inbred mouse strains display marked differences in avidity for sweet solutions due in part to genetic differences among strains. Using several techniques, we have located a number of regions throughout the genome that influence sweetener acceptance. One prominent locus regulating differences in sweetener preferences among mouse strains is the saccharin preference (Sac) locus on distal chromosome 4. Afferent responses of gustatory nerves to sweeteners also vary as a function of allelic differences in the Sac locus, suggesting that this gene may encode a sweet taste receptor. Using a positional cloning approach, we identified a gene (Tas1r3) encoding the third member of the T1R family of putative taste receptors, T1R3. Introgression by serial back-crossing of a chromosomal fragment containing the Tas1r3 allele from the high sweetener-preferring strain onto the genetic background of the low sweetener-preferring strain rescued its low sweetener-preference phenotype. Tas1r3 has two common haplotypes, one found in mouse strains with elevated sweetener preference and the other in strains relatively indifferent to sweeteners. This study, in conjunction with complimentary recent studies from other laboratories, provides compelling evidence that Tas1r3 is equivalent to the Sac locus and that the T1R3 receptor (when co-expressed with taste receptor T1R2) responds to sweeteners. However, other sweetness receptors may remain to be identified.

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“…However, rat strains with different saccharin preferences do not differ in protein sequence of T1R3 . Consistent with this, QTLs for saccharin preference in the rat were mapped to chromosomes 3, 16 and 18, but not to chromosome 5 where rat Tas1r3 resides . Therefore, rat strain differences in saccharin preferences depend on genes other than Tas1r3 .…”

Section: Within‐species Variation In Sweet Taste Preferencessupporting

confidence: 62%

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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Cited by 20 publications

References 33 publications

Derivation and Characterization of Replicate High- and Low-Alcohol Preferring Lines of Mice and a High-Drinking Crossed HAP Line

Derivation and Characterization of Replicate High- and Low-Alcohol Preferring Lines of Mice and a High-Drinking Crossed HAP Line

Genetics of sweet taste preferences

Genetics of sweet taste preferences

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