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Our lab previously established that repeated exposure to a bitter diet can increase salivary protein (SP) expression, which corresponds to an increase in acceptance of the bitter stimulus. However, this work was exclusively in male rodents, here we examine sex differences. We found that there are no differences in SP expression (experiment 1) or quinine diet acceptance (experiment 2) across stage of estrous cycle. Yet, males and females differ in feeding behaviors, SP expression, and responses to a quinine diet (experiment 3). On a quinine diet, males accepted the diet much faster than females. Males displayed a compensatory increase in meal number as meal size and rate of feeding decreased with initial exposure to a quinine diet, whereas females decreased meal size and rate of feeding with no compensation in meal number. There were sex differences in SP expression at day 14 of quinine exposure but these were gone by day 24. Both sexes increased acceptance of quinine in a brief access taste test after the feeding trial concluded. These data suggest that males and females have different patterns of bitter diet acceptance, but extended exposure to quinine diet still results in altered bitter taste responding and changes in SP profiles in females. 

Previous studies suggested that the copy number of the human salivary amylase gene,AMY1, correlates with starch-rich diets. However, evolutionary analyses are hampered by the absence of accurate, sequence-resolved haplotype variation maps. We identified 30 structurally distinct haplotypes at nucleotide resolution among 98 present-day humans, revealing that the coding sequences ofAMY1copies are evolving under negative selection. Genomic analyses of these haplotypes in archaic hominins and ancient human genomes suggest that a common three-copy haplotype, dating as far back as 800,000 years ago, has seeded rapidly evolving rearrangements through recurrent nonallelic homologous recombination. Additionally, haplotypes with more than threeAMY1copies have significantly increased in frequency among European farmers over the past 4000 years, potentially as an adaptive response to increased starch digestion. 

Abstract The peripheral taste system is more complex than previously thought. The novel taste-signaling proteins TRPM4 and PLCβ3 appear to function in normal taste responding as part of Type II taste cell signaling or as part of a broadly responsive (BR) taste cell that can respond to some or all classes of tastants. This work begins to disentangle the roles of intracellular components found in Type II taste cells (TRPM5, TRPM4, and IP3R3) or the BR taste cells (PLCβ3 and TRPM4) in driving behavioral responses to various saccharides and other sweeteners in brief-access taste tests. We found that TRPM4, TRPM5, TRPM4/5, and IP3R3 knockout (KO) mice show blunted or abolished responding to all stimuli compared with wild-type. IP3R3 KO mice did, however, lick more for glucose than fructose following extensive experience with the 2 sugars. PLCβ3 KO mice were largely unresponsive to all stimuli except they showed normal concentration-dependent responding to glucose. The results show that key intracellular signaling proteins associated with Type II and BR taste cells are mutually required for taste-driven responses to a wide range of sweet and carbohydrate stimuli, except glucose. This confirms and extends a previous finding demonstrating that Type II and BR cells are both necessary for taste-driven licking to sucrose. Glucose appears to engage unique intracellular taste-signaling mechanisms, which remain to be fully elucidated.