Mechanisms of Taste Transduction
Robert H. Cagan in Neural Mechanisms in Taste, 2020
The importance of the surface of the taste receptor cell in taste reception was clearly recognized by Renqvist.47 Subsequently, several lines of evidence had accumulated that supported his hypothesis (summarized in Reference 48). It was not until the 1970s, however, that direct evidence for specific binding of taste stimulus molecules to plasma membranes began to be presented.49–51 Central to this demonstration was the utilization of an appropriate experimental model, the channel catfish. Its extensive “externalized” taste system and generally higher sensitivity to stimuli2 than that of mammals made it possible to both prepare sufficient receptor material and measure binding experimentally because of a sufficiently high affinity for taste ligands. The findings on interactions of amino acids with these receptors are summarized in Section IV.B.
Chemosensory Influences on Eating and Drinking, and Their Cognitive Mediation
Alan R. Hirsch in Nutrition and Sensation, 2023
In other words, psychology’s longstanding measure of differential sensitivity, Weber’s fraction, is the key to working out the causal processes by which tastes and smells produce selective ingestion. Central interactions between taste receptor afferents are well recognized. These are particularly evident in subadditivity between responses to components of experimental mixtures of taste compounds. Various mathematical models of such “mixture suppression” have been proposed, from a widely used cosine function (Cain, Schiet, Olsson, and deWijk 1995) to parallel versus fan interactions in ANOVA (De Graaf, Frijters, and Van Trijp 1987; McBride 1988, 1993; McBride and Finlay 1990). Yet no specific mechanism has been proposed to justify either sort of calculation (see Schifferstein and Frijters 1993). In contrast, the concentrations of the taste compounds in the tested mixtures can be scaled on a number of discriminations from the standard in memory that was used by a response made to each sample. Then the observed values of that response can be predicted from causal processes specified by exact arithmetic (Booth under review; Booth and Freeman 1993).
Chemosensation
Emily Crews Splane, Neil E. Rowland, Anaya Mitra in Psychology of Eating, 2019
Taste receptors are located in groups of 50–100 cells within garlic-bulb-shaped structures called taste buds (Figure 5.2). About half of the cells in a taste bud are called Type I cells and serve various support functions but do not have taste receptors. Type II cells comprise about one third of cells in a taste bud and transduce sweet, umami, or bitter tastes. They do so via combinations of GPCRs: Different chemical tastants impart a particular taste sensation by activating specific receptors. Type III cells are the least numerous and do not express GPCRs but do transduce sour taste (Roper & Chaudhari, 2017). Taste buds form the sides of nipple-like structures called papillae, which appear as bumps on the surface of the tongue and other parts of the oral cavity including the palate (roof of the mouth) and throat. The main types of gustatory papillae found on the tongue are fungiform, foliate, and circumvallate and, although the densities of these papillae change across the tongue, they all are able to transduce all of the taste qualities: The myth of a tongue map, according to which different tastes were specific to tongue regions, is exactly that – a myth (Hevezi et al., 2009).
Intragastric quinine administration decreases hedonic eating in healthy women through peptide-mediated gut-brain signaling mechanisms
Published in Nutritional Neuroscience, 2019
Julie Iven, Jessica R. Biesiekierski, Dongxing Zhao, Eveline Deloose, Owen G. O’Daly, Inge Depoortere, Jan Tack, Lukas Van Oudenhove
Distinguishing bitter taste allows detection of toxic compounds in food.1 However, some people have a preference for bitter taste, depending on their sensitivity to bitter compounds, which is sex-dependent, with women on average being more sensitive.1,2 Bitter tastants (i.e. chemicals stimulating the sense of taste) are sensed via taste receptors of the taste 2 receptor family (TAS2R) class of G-protein coupled receptors, located on taste receptor cells in lingual taste buds. However, TAS2Rs are also present on enteroendocrine cells (EEC) throughout the gastrointestinal (GI) tract.3 Activation of taste receptors on EECs occurs via a chemosensory signaling pathway and results in altered secretion of GI peptide hormones involved in the regulation of food intake.4 More specifically, TAS2Rs are present on ghrelin-producing X/A-like cells in the gastric fundus, among others. Ghrelin, a 28-amino acid peptide, is the key orexigenic GI hormone as its plasma levels peak pre-prandially and decrease rapidly with food ingestion.5 Motilin, a polypeptide hormone secreted by EECs in the duodenum, jejunum, and neurons of the myenteric plexus, is the regulator of the migrating motor complex (MMC), a cyclic secretomotor pattern during the fasted state that originates in the stomach and small bowel. Plasma motilin levels fluctuate with the phases of the MMC, and motilin-induced gastric phase III contractions coincide with increases in fasting hunger ratings, pointing towards an orexigenic effect of motilin.6,7
Safety of current therapies for onychomycosis
Published in Expert Opinion on Drug Safety, 2020
Jose W. Ricardo, Shari R. Lipner
The pathogenesis of taste disturbance with terbinafine is poorly understood. It is thought that taste receptor dysfunction occurs through inhibition of cytochrome P-450 dependent enzymes[35]. As per the package insert, taste/smell disturbances may resolve within weeks of discontinuing terbinafine, but may also be prolonged (greater than 1 year) or permanent. There are 23 reported cases of permanent taste/smell disturbances [36,37,38,43], Two [39,40,42] patients had complete taste loss and one [41] had only partial, four [41] had anosmia and two [41] had partial smell loss, one [41] patient had partial loss of both taste and smell, and another one [41] had complete loss of taste and smell. For the remaining 12 cases of permanent taste/smell disturbances, the specific deficit was not described. In a case-control study of 87 patients with self-reported terbinafine-associated taste loss and 362 controls who took terbinafine without taste loss, patients with body mass index (BMI) <21 kg/m2 and those aged ≥65 years were more likely to experience taste disturbances with terbinafine, compared with patients with BMI ≥27 kg/m2 and those aged ≤35 years, respectively[44]. Therefore, patients should be warned about these uncommon but troubling side effects before terbinafine treatment is prescribed.
Individual Differences in Chemosensory Perception Amongst Cancer Patients Undergoing Chemotherapy: A Narrative Review
Published in Nutrition and Cancer, 2022
Alba Ruiz-Ceamanos, Charles Spence, Jordi Navarra
In fact, it has been estimated that 45–84% of these patients suffer from alterations to their sense of taste and somewhere between 5–60% from alterations to their sense of smell (15). Somewhat surprisingly, however, not all of those patients who suffer from alterations to their chemical senses necessarily describe them in quite the same way, nor suffer them with quite the same intensity (16). Taste alterations may, for example, include the absence of taste (ageusia), a decrease of taste sensitivity (hypogeusia), or the appereance of strange taste sensations in the absence of any flavorful inputs (phantogeusia). Other patients report an increase in the intensity of certain tastes (hypergeusia) and taste distortions when the taste receptors are activated by an external agent (dysgeusia; see 11).