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Sophorolipids (SL) are typically produced and secreted by select nonpathogenic yeast species (i.e., Candida) from renewable substrates. They are currently being used by industry on a limited basis in formulations for cleaning solutions as well as laundry and dishwashing detergents. Due to the nature of their chemical structure, it was hypothesized that SL would demonstrate taste‐sensory properties. In this study, SL were produced via fermentation on a mixed substrate platform with glucose and either palmitic acid, stearic acid, or oleic acid using Candida (currently reclassified as Starmerella) bombicola ATCC 22214. The taste properties of SL were determined using a single‐cell manual calcium imaging technique on cultured human fungiform taste papillae (HBO) cells. The results of those studies demonstrated that sweetener‐responsive HBO cells also respond to SL, and these responses are mediated by the type 1 taste receptors 3 (T1R3), because they were blocked by lactisole (a T1R3 receptor‐specific blocker). The involvement of the T1R3 receptor in SL recognition was confirmed via the chorda tympani nerve recording (CTNR) study in a (−/−) T1R3 knockout (KO) mouse model. We further demonstrated that SL are capable of blocking the bitter stimuli‐elicited responses both in HBO cells and in the CTNR study. This is the first report demonstrating that SL have taste‐sensory properties, which opens up numerous possibilities for practical applications of SL to ameliorate bitter tastes in foods and drugs and understand the potential source of dysgeusia in some patients. [ABSTRACT FROM AUTHOR]

BSTRACT 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. Copyright © 2011 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

The article discusses a study which aimed to identify the gene that accounts for the linkage of quantitative trait loci (QTL) on chromosome 7 that affect body composition, and to determine whether the QTL are specific to the weight of adipose tissue, or extends to other organs or tissues, such as bone, liver, brain, or lean mass. Findings show several associations that suggest one or more QTL specific to the weight of select tissues and organs exist on mouse chromosome 7.

Mice of the C57BL/6ByJ (B6) and 129/J (129) strains were offered different concentrations of taste solutions in 48-hr, two-bottle choice tests. In comparison with the 129 strain, the B6 strain had higher preferences for ethanol, sucrose, and citric acid. They had lower preferences for NaCl and similar preferences for capsaicin and quinine hydrochloride. These data are consistent with the hypothesis that the higher ethanol intake by B6 mice depends, in part, on higher hedonic attractiveness of its sweet taste component. [ABSTRACT FROM AUTHOR]

We have begun to characterize the genetic basis of calcium consumption. Previously, we found that the PWK/PhJ mouse strain has stronger preferences for calcium solutions than do 39 other strains, including the C57BL/6J strain (see Mouse Phenome Database, project 103). To determine the cause of this variation, we phenotyped and genotyped 481 C57BL/6J x PWK/PhJ F2 hybrids. Phenotypes included a 96-h two-bottle preference test with a choice between water and 50 mM CaCl2. Genotypes were based on 116 SSLP markers. Interval mapping revealed two quantitative trait loci (QTLs) for calcium intake. One was on proximal chromosome 16 with a peak close to Casr, an extracellular calcium receptor. This QTL supports the hypothesis that CaSR detects oral and/or circulating calcium to control calcium intake. The other was on distal chromosome 4 with a peak close to Tas1r3, the sweet receptor. Taken with confirmatory evidence, this suggests that calcium interacts with the sweet receptor to stimulate calcium intake in some strains of mice. Perhaps PWK/PhJ mice drink calcium avidly because they perceive it to be sweet. [ABSTRACT FROM AUTHOR]