SummaryBackground-Human skin emits a variety of volatile metabolites, many of them odorous. Much previous work has focused upon chemical structure and biogenesis of metabolites produced in the axillae (underarms), which are a primary source of human body odour. Nonaxillary skin also harbours volatile metabolites, possibly with different biological origins than axillary odorants.

Gustducin is a transducin-like G protein selectively expressed in taste receptor cells. The alpha subunit of gustducin (alpha-gustducin) is critical for transduction of responses to bitter or sweet compounds. We identified a G-protein gamma subunit (Ggamma13) that colocalized with alpha-gustducin in taste receptor cells. Of 19 alpha-gustducin/Ggamma13-positive taste receptor cells profiled, all expressed the G protein beta3 subunit (Gbeta3); approximately 80% also expressed Gbeta1. Gustducin heterotrimers (alpha-gustducin/Gbeta1/Ggamma13) were activated by taste cell membranes plus bitter denatonium. Antibodies against Ggamma13 blocked the denatonium-induced increase of inositol trisphosphate (IP3) in taste tissue. We conclude that gustducin heterotrimers transduce responses to bitter and sweet compounds via alpha-gustducin's regulation of phosphodiesterase (PDE) and Gbetagamma's activation of phospholipase C (PLC).

The characterization of the source of the odor in the human axillary region is not only of commercial interest but is also important biologically because axillary extracts can alter the length and timing of the female menstrual cycle. In males, the most abundant odor component is known to be E-3-methyl-2-hexenoic acid (E-3M2H), which is liberated from nonodorous apocrine secretions by axillary microorganisms. Recently, it was found that in the apocrine gland secretions, 3M2H is carried to the skin surface bound to two proteins, apocrine secretion odor-binding proteins 1 and 2 (ASOBI and ASOB2) with apparent molecular masses of 45 kDa and 26 kDa, respectively. To better understand the formation of axillary odors and the structural relationship between 3M2H and its carrier protein, the amino acid sequence and glycosylation pattern of ASOB2 were determined by mass spectrometry. Axillary secretions and odors are derived from an area of the body with exceptional odor-producing capabilities. Several types of skin glands, including apocrine, eccrine, sebaceous, and apoeccrine glands, contribute moisture and substrate to a large permanent population of cutaneous microflora (9). These consist of lipophilic and large colony diptheroids as well as micrococci. These microorganisms generate a variety of odoriferous compounds that characterize the axillary region. In vivo correlations of odor quality and axillary bacterial populations have demonstrated that the aerobic diptheroids are associated with the stronger, more distinct axillary odor (9).A number of investigations of axillary constituents have focused upon the interesting steroidal molecules found there (10, 11). Volatile odoriferous steroids such as 5a-androst-16-en-313-ol (androstenol) and 5a-androst-16-en-3-one (androstenone) as well as nonvolatile steroid sulfates were identified and quantitated by radioimmunoassay and gas chromatography/mass spectrometry (GC/MS) (10,11), The urine/muskylike odors of androstenone and androstenol were thought by some investigators to be suggestive of axillary odor (9-11). However, recent studies (12, 13) have presented both organoleptic and analytical evidence that a mixture of C6-C11, straight-chain, branched, and unsaturated acids constitute the characteristic axillary odor. In combined male samples, the E-isomer of 3-methyl-2-hexenoic acid (3M2H) is the dominant analytical component of the mixture, while in combined female samples the straight-chain acids are present in greater relative abundance (14). The Z-isomer is also present in both genders, however in different relative abundance: 10:1 (E/Z) in males (12) and 16:1 (E/Z) in females (14).More than 30 years ago, it was demonstrated that the odorless precursors of axillary odor are present in apocrine gland secretions and that the characteristic odor arises from interaction of the odorless apocrine secretion precursors with the axillary microflora (15). The water-soluble components of apocrine secretion were found to contain the odorless precursors of the characterist...

We provide evidence that PAV-TAS2R38 expression amount correlates with individual differences in bitter sensory perception and diet. The nature of this correlation calls for additional research on the molecular mechanisms associated with some individual differences in taste perception and food intake. The trial was registered at clinicaltrials.gov as NCT01399944.

Odors produced in the human female axillae are of both biological and commercial importance. Several studies have suggested that extracts from female underarm secretions can alter the length and timing of the female menstrual cycle. In addition, more than 1.6 billion dollars are spent annually on products to eliminate or mask the axillary odors. Our recent studies have determined that the characteristic axillary odors in males consist of C6-C11, saturated, unsaturated and branched acids, with (E)-3-methyl-2-hexenoic acid (3M2H) being the major compound in this mixture. The 3M2H appears to be carried to the skin surface bound to two proteins in the axillary secretions. Data reported here show that the same mixture of odorous compounds is found in female axillary secretions, with several minor qualitative differences. Separation of the female apocrine secretions into aqueous and organic soluble fractions demonstrated that 3M2H, and several other members of the acids in the characteristic odor, are released by hydrolysis with base. Electrophoretic separation of the proteins found in the aqueous phase of female apocrine secretions revealed a pattern identical to that seen in males. The qualitative similarity of the acidic constituents making up the characteristic axillary odors of both females and males as well as the proteins present in the aqueous phase suggest a similar origin for axillary odors in both sexes.

In spite of the coexistence of saliva and taste in the oral cavity, an understanding of their interactions is still incomplete. Saliva has modulating effects on sour, salt, and the monosodium-glutamate-induced savory or umami taste. It has a diminishing effect on sour taste as a result of the buffering by salivary bicarbonate. It probably also contributes to the umami taste with endogenous salivary glutamate levels. Salt taste is detected only when above salivary sodium-chloride concentrations; thus saliva influences salt taste threshold levels. It also provides the ionic environment for taste cells, probably critical in signal transduction. Salivary flow rate and composition are influenced by the type of taste stimuli. In general, sour taste, elicited by citric acid or sour food, induces the highest flow rate and Na+ concentrations, while salt gives rise to high protein and Ca2+ concentrations. Stimulation with the four basic taste modalities (sour, sweet, salty, and bitter), however, does not increase the relative proportion of any of the salivary proteins. This review examines the literature on the interactions of saliva with taste, and the effect of taste on salivary composition. The possible role of the von Ebner's salivary glands and the role of saliva as a chemical cue are also discussed.

Recently completed studies from our laboratories have demonstrated that the characteristic human male axillary odors consist of C6 to C11 normal, branched, and unsaturated aliphatic acids, with (E)-3-methyl-2-hexenoic acid being the most abundant. To investigate the mechanism by which the odor is formed, it is necessary to determine the nature of the odorless precursor(s) found in the apocrine secretion which is converted by the cutaneous microorganisms to the characteristic axillary odor. Pooled apocrine secretion was obtained from several male volunteers by intracutaneous injection of epinephrine. Partitioning this secretion into aqueous and organic soluble fractions was followed by hydrolysis of each fraction with NaOH or incubation with axillary microorganisms (cutaneous lipophilic corynebacterium). Analysis by gas chromatography/mass spectrometry (GC/MS) revealed the presence of (E)- and (Z)-3-methyl-2-hexenoic acid in the aqueous phase hydrolysate and aqueous phase incubated with bacteria; however, only a trace amount was seen in the resultant organic phase mixtures. These results suggest that a water-soluble precursor(s) is converted by the axillary flora to the characteristic axillary odors.

Current evidence points to the existence of multiple processes for bitter taste transduction. Previous work demonstrated involvement of the polyphosphoinositide system and an alpha-gustducin (Galpha(gust))-mediated stimulation of phosphodiesterase in bitter taste transduction. Additionally, a taste-enriched G protein gamma-subunit, Ggamma(13), colocalizes with Galpha(gust) and mediates the denatonium-stimulated production of inositol 1,4,5-trisphosphate (IP(3)). Using quench-flow techniques, we show here that the bitter stimuli, denatonium and strychnine, induce rapid (50-100 ms) and transient reductions in cAMP and cGMP and increases in IP(3) in murine taste tissue. This decrease of cyclic nucleotides is inhibited by Galpha(gust) antibodies, whereas the increase in IP(3) is not affected by antibodies to Galpha(gust). IP(3) production is inhibited by antibodies specific to phospholipase C-beta(2) (PLC-beta(2)), a PLC isoform known to be activated by Gbetagamma-subunits. Antibodies to PLC-beta(3) or to PLC-beta(4) were without effect. These data suggest a transduction mechanism for bitter taste involving the rapid and transient metabolism of dual second messenger systems, both mediated through a taste cell G protein, likely composed of Galpha(gust)/beta/gamma(13), with both systems being simultaneously activated in the same bitter-sensitive taste receptor cell.