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[Assessment of the correlation between taste and smell functioning].

UNLABELLED: There are few studies examining relationship between taste and smell. However their clinical unity is more often indicated. Smell perception abnormalities cause modification in taste of food intensity, disabling perception of taste as a consequence of taste's sniffing failure. Thus disturbances of these senses, which often commonly coexist could cause great discomfort in patients, however taste sense is estimated as less important comparing to smell sense. The aim of that study was to compare the taste perception in patients with normal smell function and patients with hyposmia and anosmia. There was analyzed correlation between the patients' subjective estimation of smell and taste senses and results of gustometry and olfactometry examinations. MATERIAL AND METHOD: there were indicated three groups of patients based on smell examination with usage of Elsberga--Levy'ego olfactometr in Pruszewicz modification. The first group included patients with normosmia, the second--patients with hyposmia or anosmia related to every smell, the third--patients with hyposmia on few smells and normal smell feeling of others. The Bornstein's method gustometry modified by us was performed for all groups. Moreover patients presented their subjective estimation of smell and taste senses. All results were statistically analyzed, taking into consideration results with alpha < or = 0.05. RESULTS: All (100%) patients with normosmia correctly identified sour, bitter and salty tastes, while only 53% of patients with hyposmia and anosmia got similar results. However 76.5% of patients from the second group subjectively estimated their sense of taste as a normal perception. CONCLUSIONS: Patients with smell disturbances significantly more often have abnormalities in taste perception than patients with normosmia and their subjective estimation of taste and smell senses is much more different than gustometry and olfactometry results.

Adult↗

Taste fiber responses during reinnervation of fungiform papillae.

Crushing or transecting the chorda tympani nerve of the gerbil (Meriones unguiculatus) caused ipsilateral degeneration of taste buds in the fungiform papillae. In less than two weeks some taste fibers regenerated into the tongue and formed new taste buds and receptor cells. The recovery process was evaluated electrophysiologically in 53 gerbils by acute recording proximal to the nerve injury site. Initially the chorda tympani was electrically silent. In gerbils tested at later times spontaneous activity appeared. This was followed by responses to pressure on the tongue. Taste responses returned as early as day 11. The receptive field of regenerated taste fibers was limited to a small number of fungiform papillae. Taste responses were always associated with the presence of one or more taste buds in the receptive field. Taste buds identified as responsive to chemicals contained some fusiform cells. We found that the taste responses of single fiber, few-fiber and multi-unit preparations reflected the diversity of responses found in normal taste axons as determined by recording from 26 normal single fibers and 27 normal whole nerves. The early emergence of a variety of fiber types and responses to many chemicals in regeneration is inconsistent with the proposition that the relative chemical responsiveness of a receptor cell is strictly a function of its age; the response of a given young taste receptor is not necessarily limited to a few of the standard taste stimulants.

Animals↗

Clinical applications and mechanism of intravenous taste tests.

It is well known that there are two ways to measure human blood circulation time: the arm-to-lung and the arm-to-tongue method. The decholin (20% dehydrocholic acid) test is usually used to measure the arm-to-tongue circulation time. In this study, this procedure was used to examine taste function. Findings on the clinical application of this intravenous taste test using decholin and a study on the mechanism of venous taste perception are reported here. The following method was used: Five ml of 20% decholin were injected into the right cubital vein over a 10-sec period and the latent time, the duration, the quality of the taste sensation and the region of the tongue where the taste appeared were noted. The results were as follows: 1) In dysgeusic subjects, the latent period was longer, and the duration of the taste sensation was shorter than in normal subjects (p is less than 0.01, p is less than 0.05). 2) Some of the dysgeusic subjects perceived the taste as other than bitter; their prognosis of taste dysfunction tended to be worse than that of other subjects. 3) Some of the dysgeusic subjects perceived the taste in regions of the tongue other than the bilateral edges or over the entire tongue; their prognosis of taste dysfunction tended to be worse than that of other subjects. 3) Some of the dysgeusic subjects perceived the taste in regions of the tongue other than bilateral edges or over the entire tongue; their prognosis tended to be worse than that of other subjects. In addition, photofluorograms of the tongue were taken to clarify the mechanism of intravenous taste; the time needed for fluorescence to appear in the fungiform papillae and their diffusion form in the papillae were observed and investigated.

Adolescent↗

Adenylyl cyclase expression and modulation of cAMP in rat taste cells.

cAMP is a second messenger implicated in sensory transduction for taste. The identity of adenylyl cyclase (AC) in taste cells has not been explored. We have employed RT-PCR to identify the AC isoforms present in taste cells and found that AC 4, 6, and 8 are expressed as mRNAs in taste tissue. These proteins are also expressed in a subset of taste cells as revealed by immunohistochemistry. Alterations of cAMP concentrations are associated with transduction of taste stimuli of several classes. The involvement of particular ACs in this modulation has not been investigated. We demonstrate that glutamate, which is a potent stimulus eliciting a taste quality termed umami, causes a decrease in cAMP in forskolin-treated taste cells. The potentiation of this response by inosine monophosphate, the lack of response to d-glutamate, and the lack of response to umami stimuli in nonsensory lingual epithelium all suggest that the cAMP modulation represents umami taste transduction. Because cAMP downregulation via ACs can be mediated through Galpha(i) proteins, we examined the colocalization of the detected ACs with Galpha(i) proteins and found that 66% of AC8 immunopositive taste cells are also positive for gustducin, a taste-specific Galpha(i) protein. Whether AC8 is directly involved in signal transduction of umami taste remains to be established.

1-Methyl-3-isobutylxanthine↗

Interaction of saliva and taste.

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.

Humans↗

The sense of taste: neurobiology, aging, and medication effects.

The sense of taste is an oral chemical sense in mammals that is involved in the choice of foods. Initial transduction of taste stimuli occurs in taste buds, which are distributed in four discrete fields in the oral cavity. Medications can affect the taste buds and ion channels in taste-bud cell membranes involved in stimulus transduction. The sense of taste gradually declines with aging, with bitter taste most affected. Neural circuits that mediate taste in primates include cranial nerves VII, IX, and X, the solitary nucleus in the brain stem, the ventroposteromedial nucleus of the thalamus, and the insular-opercular cortex. The central taste pathways process taste information about sweet, salty, sour, and bitter stimuli serially and in parallel. Medications associated with "metallic" dysgeusia and taste losses affect the taste system via unknown mechanisms.

Aging↗

Immunocytochemical evidence for co-expression of Type III IP3 receptor with signaling components of bitter taste transduction.

BACKGROUND: Taste receptor cells are responsible for transducing chemical stimuli into electrical signals that lead to the sense of taste. An important second messenger in taste transduction is IP3, which is involved in both bitter and sweet transduction pathways. Several components of the bitter transduction pathway have been identified, including the T2R/TRB taste receptors, phospholipase C beta2, and the G protein subunits alpha-gustducin, beta3, and gamma13. However, the identity of the IP3 receptor subtype in this pathway is not known. In the present study we used immunocytochemistry on rodent taste tissue to identify the IP3 receptors expressed in taste cells and to examine taste bud expression patterns for IP3R3. RESULTS: Antibodies against Type I, II, and III IP3 receptors were tested on sections of rat and mouse circumvallate papillae. Robust cytoplasmic labeling for the Type III IP3 receptor (IP3R3) was found in a large subset of taste cells in both species. In contrast, little or no immunoreactivity was seen with antibodies against the Type I or Type II IP3 receptors. To investigate the potential role of IP3R3 in bitter taste transduction, we used double-label immunocytochemistry to determine whether IP3R3 is expressed in the same subset of cells expressing other bitter signaling components. IP3R3 immunoreactive taste cells were also immunoreactive for PLCbeta2 and gamma13. Alpha-gustducin immunoreactivity was present in a subset of IP3R3, PLCbeta2, and gamma13 positive cells. CONCLUSIONS: IP3R3 is the dominant form of the IP3 receptor expressed in taste cells and our data suggest it plays an important role in bitter taste transduction.

Animals↗

Roles of chemical mediators in the taste system.

Recent advances in neural mechanisms of taste are reviewed with special reference to neuroactive substances. In the first section, taste transduction mechanisms of basic tastes are explained in two groups, whether taste stimuli directly activate ion channels in the taste cell membrane or they bind to cell surface receptors coupled to intracellular signaling pathways. In the second section, putative transmitters and modulators from taste cells to afferent nerves are summarized. The candidates include acetylcholine, catecholamines, serotonin, amino acids and peptides. Studies favor serotonin as a possible neuromodulator in the taste bud. In the third section, the role of neuroactive substances in the central gustatory pathways is introduced. Excitatory and inhibitory amino acids (e.g., glutamate and GABA) and peptides (substance P and calcitonin gene-related peptide) are proved to play roles in transmission of taste information in both the brainstem relay and cortical gustatory area. In the fourth section, conditioned taste aversion is introduced as a model to study gustatory learning and memory. Pharmacobehavioral studies to examine the effects of glutamate receptor antagonists and protein kinase C inhibitors on the formation of conditioned taste aversion show that both glutamate and protein kinase C in the amygdala and cortical gustatory area play essential roles in taste aversion learning. Recent molecular and genetic approaches to disclose biological mechanisms of gustatory learning are also introduced. In the last section, behavioral and pharmacological approaches to elucidate palatability, taste pleasure, are described. Dopamine, benzodiazepine derivatives and opioid substances may play some roles in evaluation of palatability and motivation to ingest palatable edibles.

Animals↗

Epithelial Na+ channel subunits in rat taste cells: localization and regulation by aldosterone.

Amiloride-sensitive Na+ channels play an important role in transducing Na+ salt taste. Previous studies revealed that in rodent taste cells, the channel shares electrophysiological and pharmacological properties with the epithelial Na+ channel, ENaC. Using subunit-specific antibodies directed against alpha, beta, and gamma subunits of rat ENaC (rENaC), we observed cytoplasmic immunoreactivity for all three subunits in nearly all taste cells of fungiform papillae, and in about half of the taste cells in foliate and vallate papillae. The intensity of labeling in cells of vallate papillae was significantly lower than that of fungiform papillae, especially for beta and gamma subunits. Dual localization experiments showed that immunoreactivity for the taste cell-specific G protein, gustducin, occurs in a subset ofrENaC positive taste cells. Aldosterone is known to increase the amiloride sensitivity of the NaCl taste response. In our study, increases in blood aldosterone levels enhanced the intensity of apical immunoreactivity for beta and gamma rENaC in taste cells of all papillae. In addition, whole cell recordings from isolated taste cells showed that in fungiform papillae, aldosterone increased the number of amiloride-sensitive taste cells and enhanced the current amplitude. In vallate taste cells, which are normally unresponsive to amiloride, aldosterone treatment induced an amiloride sensitive current in about half of the cells. Immunoreactivity for rENaC subunits also was present in nonsensory epithelial cells, especially in the anterior portion of the tongue. In addition, immunoreactivity for all subunits, but especially beta and gamma, was associated with some nerve fibers innervating taste papillae. These extragustatory sites of rENaC expression may indicate a role for this channel in paracellular transduction of sodium ions.

Aldosterone↗

Variation in human fungiform taste bud densities among regions and subjects.

Taste sensitivity is known to vary among regions of the tongue and between subjects. The distribution of taste buds on the human tongue is examined in this report to determine if interregional and intersubject variation of taste bud density might account for some of the variation in human taste sensitivity. The subjects were ten males, aged 22-80 years, who died from acute trauma or an acute cardiovascular episode. Specimens were obtained as anatomical gifts or from autopsy. A sample of tissue about 1 cm2 was taken from the tongue tip and midlateral region; frozen sections were prepared for light microscopy; and serial sections were examined by light microscopy to count the taste buds. The average taste bud (tb) density on the tongue tip was 116 tb/cm2 with a range from 3.6 to 514 among subjects. The number of gustatory papillae on the tip averaged 24.5 papillae/cm2 with a range from 2.4 to 80. Taste bud density in the midregion averaged 25.2 tb/cm2 (range: 0-85.9), and the mean number of gustatory papillae was 8.25/cm2 (range: 0-28). The mean number of taste buds per papilla was 3.8 +/- 2.2 (s.d.) on the tip and 2.6 +/- 1.5 (s.d.) on the midregion. Subjects with the highest taste bud densities on the tip also had the highest densities in the midregion and the highest number of taste buds per papilla. Taste bud density was 4.6 times higher on the tip than the midregion, which probably accounts for some of the regional difference in taste sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Taste bud distribution in the rat pharynx and larynx.

The present study evaluated the number and distribution of taste buds in the rat pharynx and larynx using light microscopic techniques. The average number of taste buds in this region was 141.9 (S.D. = 29.4, n = 10). Pharyngeal and laryngeal taste buds could be grouped into three subpopulations: those associated with laryngeal structures (LA), the nasopharynx (NP), or the palatopharyngeal eminence (PE). Laryngeal taste buds were most numerous (mean = 103.2, S.D. = 23.6). They were observed on the laryngeal surface of the epiglottis and extended caudally along the aryepiglottic folds, reaching peak density at the caudal extreme of the folds. Further caudally, when the larynx and rostral esophagus separated, taste bud density decreased sharply. Fewer taste buds were associated with the NP (mean = 31.9, S.D. = 13.7) or PE (mean = 6.8, S.D. = 4.0) and taste bud density in these subpopulations peaked at the anterior border of the nasopharyngeal hiatus. Taste buds in the rat larynx and pharynx account for 10% all taste buds in this species, a proportion similar to that accounted for by taste buds on the soft palate. Taste buds in this region appear to be ideally situated for protecting the airway during accidental aspiration of food or fluids. Most pharyngeal and laryngeal taste buds are unlikely to be involved in triggering normally occurring swallows, although they could be stimulated as the bolus is propelled from the oral cavity to the esophagus.

Animals↗

Immunocytochemistry of gamma-aminobutyric acid, glutamate, serotonin, and histamine in Necturus taste buds.

Little information is currently available about which neurotransmitters are involved in signal processing in the peripheral sensory organs of taste, taste buds. Synaptic contacts between taste cells and sensory axons have long been known to exist, but what substances are active at these synapses is not known. Our objective in this study was to test for the presence of the neurotransmitter candidates, GABA, glutamate, serotonin, and histamine in taste buds of Necturus maculosus. Light microscopic immunocytochemical techniques were used to investigate the location of these substances in taste buds and surrounding epithelium. GABA and glutamate were detected in nerve fibers that innervate the taste buds, and, to a substantially lesser extent, in fine, varicose axons that penetrated the surrounding nontaste epithelium. Serotonin immunostaining was strong in basal cells in frog taste discs but was only faintly detected in Necturus taste buds. Histamine was not detected at all in taste buds. We conclude that amino acid neurotransmission may be involved in taste mechanisms and that monoamines may also play a role in chemosensory transduction in the taste bud. On the basis of our inability to detect histamine with immunocytochemical techniques, we conclude that this substance is unlikely to be a major neurotransmitter in Necturus taste buds.

Animals↗

HVEM ultrastructural analysis of mouse fungiform taste buds, cell types, and associated synapses.

We have used high voltage electron microscopy and computer-generated three-dimensional reconstructions from serial sections to elucidate the structure of taste bud cells and their associated synapses in fungiform taste buds of the mouse. Five fungiform taste buds (two of which were serially sectioned) were examined with the high-voltage electron microscope (HVEM). We identified the synaptic connections from taste cells onto sensory nerve fibers and classified the presynaptic taste cells based on previously established ultrastructural criteria. From those data we have distinguished dark, intermediate, and light cells in murine fungiform taste buds. Synapses in murine fungiform taste buds are fewer in number, but contain many more vesicles than synapses in either foliate or circumvallate taste buds. Synapses in mouse circumvallate and foliate taste buds typically contain a few to several synaptic vesicles per section, whereas fungiform synapses may have in excess of 100 vesicles per profile. The significance of these differences in the numbers of synapses and synaptic structure between fungiform and circumvallate/foliate synapses is not known. Based on the small number of synapses observed in fungiform taste buds, we speculate that fungiform taste buds have only a few cells transducing sensory stimuli at any given time. Alternatively, communication of sensory information from the taste receptor cells to the afferent nerve fibers may be mediated by some other mechanism(s) in addition to classical chemical synapses.

Animals↗

Systematic studies of structure and physiological activity of alapyridaine. A novel food-born taste enhancer.

By application of taste dilution analysis (+)-(S)-1-(1-carboxyethyl)-5-hydroxy-2-(hydroxymethyl)-pyridinium inner salt was recently successfully identified as a multimodal taste enhancer in beef bouillon. While being taste-less on its own, this so-called alapyridaine was found to intensify the human perception of sweet, salty, and umami taste. To gain information on the molecular requirements of this novel class of taste enhancer, a range of structurally related pyridinium betaines were synthesized, purified, and their physiological activities sensorially evaluated. Removal or modification of the hydroxyl and the hydroxymethyl group, respectively, induced a loss in bioactivity, thus indicating the 2-(hydroxymethyl)-5-hydroxypyridinium moiety as an essential structural element for taste enhancement. Regarding the amino substituent, neither the prolongation or removal of the alkyl chain or the carboxy function in the 1-(1-carboxy-2-ethyl)-moiety, nor the incorporation of an additional carboxy function led to any active derivative, thus demonstrating that also the structure of the nitrogen substituent is rather conserved for taste enhancement. But substitution of the methyl group by a benzyl group yielded a compound showing similar taste enhancing activities as found for alapyridaine. Interestingly, additional insertion of glycine between the 1-(1-carboxy-2-phenylethyl)-moiety and the pyridinium ring resulted in a compound eliciting comparable taste enhancing effects as shown for the compound lacking the glycine spacer. In contrast to these multimodal taste enhancers, substitution of the alanine moiety in alapyridaine by an arginine moiety revealed an one-dimensional taste enhancer exclusively increasing the human sensitivity for salty taste.

Alanine↗

Immunohistochemical distribution of CD44 and some of its isoforms during human taste bud development.

Taste buds are accumulations of elongated bipolar cells situated on lingual papillae. The factors that determine the sites where a taste bud may develop are largely obscure, although it is known that the early invasion of nerve fibers plays one of the key roles in taste bud development and maturation. The conditions under which taste bud primordium cells develop are influenced by the interaction between epithelial cells and extracellular matrix molecules of the mesenchyma, such as hyaluronan. Thus, we investigated immunohistochemically the distribution pattern of the receptor for hyaluronan, CD44s, and its epithelial variant isoforms CD44v6 and CD44v9, in taste buds of human embryonic, fetal, perinatal, and adult tongues. Furthermore, we wanted to determine the temporal and spatial relationships of CD44 to sensory innervation of taste bud primordia. In early gestational stages (weeks 7-9), CD44 and its isoforms are expressed on membranes of apical perigemmal (marginal) cells covering taste bud primordia. It seems that CD44 serves as a marker for marginal cells (perigemmal cells) in early developmental stages. The expression of CD44 follows rather than precedes the invasion of sensory nerve fibers and the development of taste bud primordia (weeks 7-8). In new-born and adult taste bud cells, only the standard molecule, CD44s, is expressed; the variant isoforms, CD44v6 and CD44v9, occur only in the adjacent epithelium. From these results it is likely that marginal cells are of the utmost importance for the development and maturation of taste buds. We presume that CD44 is involved in local binding, reuptake, and degradation of hyaluronan in the early stages of taste bud formation. CD44 probably does not induce the transformation of epithelial cells into taste bud primordial cells. What is more, CD44 may change its function in the course of developmental events.

Adult↗

Persistence and calcium-dependent ATPase staining of denervated fungiform taste buds in the hamster.

Some fungiform taste buds in the hamster have been previously shown to persist for indefinite periods when deprived of their gustatory, chorda tympani (CT), innervation or both their CT and their trigeminal, lingual nerve, innervation (CT-L). The properties and numbers of persisting fungiform taste buds were examined 1 or 3 weeks after permanent CT or combined CT-L nerve cuts. The purpose was to reveal the status of taste buds at a time (3 weeks) when regenerating nerve fibres would normally be expected to reinnervate the epithelium. Denervated taste buds retain many normal characteristics including the pattern of histochemical staining for ectocalcium-dependent ATPase (Ca-ATPase). Taste-bud cells (including basal cells) have an intensely Ca-ATPase stained core surrounded by lightly stained peripheral cells. The Ca-ATPase stain was used to help identify and to define the size of the taste-bud core in denervated taste buds. Following CT-L or CT denervation most taste buds persisted; however the size of the taste-bud core was dramatically reduced. Fungiform taste buds differed in size based on their location in one of three tongue regions. The percentage decrease in size after denervation was also region specific and about the same for CT-L or CT cuts, suggesting that trigeminal fibres have no trophic effect on taste buds. However, trigeminal denervation caused a reduction in the number of persisting taste buds relative to CT denervation alone, which may be due to damage because of the loss of somatosensation.

Animals↗

Immunohistochemical localization of neuron-specific enolase and calcitonin gene-related peptide in pig taste papillae.

Immunoreactivity to neuron-specific enolase (NSE), a specific neuronal marker, and calcitonin gene-related peptide (CGRP) was localized in lingual taste papillae in the pigs. Sequential staining for NSE and CGRP by an elution technique allowed the identification of neuronal subpopulations. NSE-staining revealed a large neuronal network within the subepithelial layer of all taste papillae. NSE-positive fibers then penetrated the epithelium as isolated fibers, primarily in the foliate and circumvallate papillae, or as brush-shaped units formed by a multitude of fibers, especially in the fungiform papillae and in the apical epithelium of the circumvallate papilla. Taste buds of any type of taste papillae were found to express a dense subgemmal/intragemmal NSE-positive neuronal network. CGRP-positive nerve fibers were numerous in the subepithelial layer of all three types of taste papillae. In the foliate and circumvallate papillae, these fibers penetrated the epithelium to form extragemmal and intragemmal fibers, while in the fungiforms, they concentrated almost exclusively in the taste buds as intragemmal nerve fibers. Intragemmal NSE- and CGRP-positive fiber populations were not readily distinguishable by typical neural swellings as previously observed in the rat. The NSE-positive neuronal extragemmal brushes never expressed any CGRP-like immunoreactivity. Even more surprising, fungiform taste buds, whether richly innervated by or devoid of NSE-positive intragemmal fibers, always harboured numerous intragemmal CGRP-positive fibers. Consequently, NSE is not a general neuronal marker in porcine taste papillae. Our observations also suggest that subgemmal/intragemmal NSE-positive fibers are actively involved in synaptogenesis within taste buds. NSE-positive taste bud cells were found in all three types of taste papillae. CGRP-positive taste bud cells were never observed.

Animals↗

Effects of streptozotocin-induced diabetes on taste buds in rat vallate papillae.

Some studies have documented taste changes in patients with diabetes mellitus (DM). In order to understand the relationships between taste disorders caused by DM and the innervation and morphologic changes in the taste buds, we studied the vallate papillae and their taste buds in rats with DM. DM was induced in these rats with streptozotocin (STZ), which causes the death of beta cells of the pancreas. The rats were sacrificed and the vallate papillae were dissected for morphometric and quantitative immunohistochemical analyses. The innervations of the vallate papillae and taste buds in diabetic and control rats were detected using immunohistochemistry employing antibodies directed against protein gene product 9.5 (PGP 9.5) and calcitonin gene-related peptide (CGRP). The results showed that PGP 9.5- and CGRP-immunoreactive nerve fibers in the trench wall of diabetic vallate papillae, as well as taste cells in the taste buds, gradually decreased both intragemmally and intergemmally. The morphometry revealed no significant difference in papilla size between the control and diabetic groups, but there were fewer taste buds per papilla (per animal). The quantification of innervation in taste buds of the diabetic rats supported the visual assessment of immunohistochemical labeling, that the innervation of taste cells was significantly reduced in diabetic animals. These findings suggest that taste impairment in diabetic subjects may be caused by neuropathy defects and/or morphological changes in the taste buds.

Animals↗