The tongue is covered with thousands of small bumps calledpapillae, which are visible to thenaked eye.[2] Within each papilla are hundreds of taste buds.[1][4] The exceptions to this is thefiliform papillae that do not contain taste buds. There are between 2000 and 5000[5] taste buds that are located on the back and front of the tongue. Others are located on the roof, sides and back of the mouth, and in thethroat. Each taste bud contains 50 to 100 taste receptor cells.
Taste receptors in the mouth sense the five basic tastes:sweetness,sourness,saltiness,bitterness, andsavoriness (also known assavory orumami).[1][2][6][7] Scientific experiments have demonstrated that these five tastes exist and are distinct from one another. Taste buds are able to tell different tastes apart when they interact with different molecules or ions. Sweetness, savoriness, and bitter tastes are triggered by the binding of molecules toG protein-coupled receptors on thecell membranes of taste buds. Saltiness and sourness are perceived whenalkali metals orhydrogenions meet taste buds, respectively.[8][9]
As the gustatory system senses both harmful and beneficial things, all basic tastes bring either caution or craving depending upon the effect the things they sense have on the body.[13] Sweetness helps to identify energy-rich foods, while bitterness warns people of poisons.[14]
Among humans, taste perception begins to fade duringageing, tongue papillae are lost, andsaliva production slowly decreases.[15] Humans can also have distortion of tastes (dysgeusia). Not allmammals share the same tastes: somerodents can tastestarch (which humans cannot),cats cannot taste sweetness, and several othercarnivores, includinghyenas,dolphins, andsea lions, have lost the ability to sense up to four of their ancestral five basic tastes.[16]
The gustatory system allows animals to distinguish between safe and harmful food and to gauge different foods' nutritional value.Digestive enzymes in saliva begin to dissolve food into base chemicals that are washed over the papillae and detected as tastes by the taste buds. The tongue is covered with thousands of small bumps calledpapillae, which are visible to the naked eye. Within each papilla are hundreds of taste buds.[4] The exception to this are thefiliform papillae, which do not contain taste buds. There are between 2,000 and 5,000[5] taste buds that are located on the back and front of the tongue. Others are located on the roof, sides and back of the mouth, and in the throat. Each taste bud contains 50 to 100 taste-receptor cells.
The five specific tastes received bytaste receptors are saltiness,sweetness, bitterness, sourness, andsavoriness (often known by its Japanese nameumami, which translates to 'deliciousness').
As of the early 20th century, Western physiologists and psychologists believed that there were four basic tastes: sweetness, sourness, saltiness, and bitterness. The concept of a "savory" taste was not present in Western science at that time, but was postulated in Japanese research.[17]
One study found that salt and sour taste mechanisms both detect, in different ways, the presence ofsodium chloride (salt) in the mouth. Acids are also detected and perceived as sour.[18] The detection of salt is important to many organisms, but especially mammals, as it serves a critical role in ion and waterhomeostasis in the body. It is specifically needed in themammalian kidney as an osmotically active compound that facilitates passive re-uptake of water into the blood.[citation needed] Because of this, salt elicits a pleasant taste in most humans.
Sour and salt tastes can be pleasant in small quantities, but in larger quantities become more and more unpleasant to taste. For sour taste, this presumably is because the sour taste can signal under-ripe fruit, rotten meat, and other spoiled foods, which can be dangerous to the body because of bacteria that grow in such media. Additionally, sour taste signalsacids, which can cause serious tissue damage.
Sweet taste signals the presence ofcarbohydrates in solution.[citation needed] Since carbohydrates have a very highcalorie count (saccharides have many bonds, therefore much energy),[citation needed] they are desirable to the human body, which evolved to seek out the highest-calorie-intake foods.[citation needed] They are used as direct energy (sugars) and storage of energy (glycogen). Many non-carbohydrate molecules trigger a sweet response, leading to the development of many artificial sweeteners, includingsaccharin,sucralose, andaspartame. It is still unclear how these substances activate the sweet receptors and what adaptative significance this has had.
The savory taste (known in Japanese asumami), identified by Japanese chemistKikunae Ikeda, signals the presence of theamino acidL-glutamate. The amino acids in proteins are used in the body to build muscles and organs, and to transport molecules (hemoglobin),antibodies, and the organic catalysts known asenzymes. These are all critical molecules, and it is important to have a steady supply of amino acids; consequently, savory tastes trigger a pleasurable response, encouraging the intake ofpeptides andproteins.
Pungency (piquancy or hotness) had traditionally been considered a sixth basic taste.[19] In 2015, researchers suggested a new basic taste offatty acids called "fat taste",[20] although "oleogustus" and "pinguis" have both been proposed as alternate terms.[21][22]
The diagram above depicts the signal transduction pathway of the sweet taste. Object A is a taste bud, object B is one taste cell of the taste bud, and object C is the neuron attached to the taste cell. I. Part I shows the reception of a molecule. 1. Sugar, the first messenger, binds to a protein receptor on the cell membrane. II. Part II shows the transduction of the relay molecules. 2. G Protein-coupled receptors, second messengers, are activated. 3. G Proteins activate adenylate cyclase, an enzyme, which increases the cAMP concentration. Depolarization occurs. 4. The energy, from step 3, is given to activate the K+, potassium, protein channels.III. Part III shows the response of the taste cell. 5. Ca+, calcium, protein channels is activated.6. The increased Ca+ concentration activates neurotransmitter vesicles. 7. The neuron connected to the taste bud is stimulated by the neurotransmitters.
Sweetness, usually regarded as a pleasurable sensation, is produced by the presence ofsugars and substances that mimic sugar. Sweetness may be connected toaldehydes andketones, which contain acarbonyl group. Sweetness is detected by a variety ofG protein coupled receptors (GPCR) coupled to theG proteingustducin found on thetaste buds. At least two different variants of the "sweetness receptors" must be activated for the brain to register sweetness. Compounds the brain senses as sweet are compounds that can bind with varying bond strength to two different sweetness receptors. These receptors are T1R2+3 (heterodimer) and T1R3 (homodimer), which account for all sweet sensing in humans and animals.[23]
Taste detection thresholds for sweet substances are rated relative tosucrose, which has an index of 1.[24][25] The average human detection threshold for sucrose is 10 millimoles per liter. Forlactose it is 30 millimoles per liter, with a sweetness index of 0.3,[24] and5-nitro-2-propoxyaniline 0.002 millimoles per liter. "Natural" sweeteners such assaccharides activate the GPCR, which releasesgustducin. The gustducin then activates the moleculeadenylate cyclase, which catalyzes the production of the moleculecAMP, or adenosine 3', 5'-cyclic monophosphate. This molecule closes potassium ion channels, leading to depolarization and neurotransmitter release. Synthetic sweeteners such assaccharin activate different GPCRs and induce taste receptor cell depolarization by an alternate pathway.
The diagram depicts the signal transduction pathway of the sour or salty taste. Object A is a taste bud, object B is a taste receptor cell within object A, and object C is the neuron attached to object B. I. Part I is the reception of hydrogen ions or sodium ions. 1. If the taste is sour, H+ ions, from acidic substances, pass through H+ channels. Depolarization takes place II. Part II is the transduction pathway of the relay molecules. 2. Cation, such as K+, channels are opened. III. Part III is the response of the cell. 3. An influx of Ca+ ions is activated. 4. The Ca+ activates neurotransmitters. 5. A signal is sent to the neuron attached to the taste bud.
Sourness is the taste that describesacidity. The sourness of substances is rated relative to dilutehydrochloric acid, which has a sourness index of 1. By comparison,tartaric acid has a sourness index of 0.7,citric acid an index of 0.46, andcarbonic acid an index of 0.06.[24][25]
Sour taste is detected by a small subset of cells that are distributed across all taste buds called Type III taste receptor cells. H+ ions (protons) that are abundant in sour substances can directly enter the Type III taste cells through a proton channel.[26] This channel was identified in 2018 asotopetrin 1 (OTOP1).[27] The transfer of positive charge into the cell can itself trigger an electrical response. Some weak acids such as acetic acid can also penetrate taste cells; intracellular hydrogen ions inhibit potassium channels, which normally function to hyperpolarize the cell. By a combination of direct intake of hydrogen ions through OTOP1 ion channels (which itself depolarizes the cell) and the inhibition of the hyperpolarizing channel, sourness causes the taste cell to fire action potentials and release neurotransmitter.[28]
"Saltiness" redirects here. For saltiness in water, seeSalinity.
Saltiness taste seems to have two components: a low-salt signal and a high-salt signal. The low-salt signal causes a sensation of deliciousness, while the high-salt signal typically causes the sensation of "too salty".[30]
The low-salt signal is understood to be caused by theepithelial sodium channel (ENaC), which is composed of three subunits. ENaC in the taste cells allow sodiumcations to enter the cell. This on its own depolarizes the cell, and opensvoltage-dependent calcium channels, flooding the cell with positive calcium ions and leading toneurotransmitter release. ENaC can be blocked by the drugamiloride in many mammals, especially rats. The sensitivity of the low-salt taste to amiloride in humans is much less pronounced, leading to conjecture that there may be additional low-salt receptors besides ENaC to be discovered.[30]
A number of similar cations also trigger the low salt signal. The size oflithium andpotassium ions most closely resemble those of sodium, and thus the saltiness is most similar. In contrast,rubidium andcaesium ions are far larger, so their salty taste differs accordingly.[citation needed] The saltiness of substances is rated relative to sodium chloride (NaCl), which has an index of 1.[24][25] Potassium, aspotassium chloride (KCl), is the principal ingredient insalt substitutes and has a saltiness index of 0.6.[24][25]
Othermonovalentcations, e.g.ammonium (NH4+), anddivalent cations of thealkali earth metal group of theperiodic table, e.g. calcium (Ca2+), ions generally elicit a bitter rather than a salty taste even though they, too, can pass directly through ion channels in the tongue, generating anaction potential. But the chloride of calcium is saltier and less bitter than potassium chloride, and is commonly used in pickle brine instead of KCl.[citation needed]
The high-salt signal is poorly understood. This signal is not blocked by amiloride in rodents. Sour and bitter cells trigger on high chloride levels, but the specific receptor is unidentified.[30]
The diagram depicted above shows the signal transduction pathway of the bitter taste. Bitter taste has many different receptors and signal transduction pathways. Object A is a taste bud, object B is one taste cell, and object C is a neuron attached to object B. I. Part I is the reception of a molecule.1. A bitter substance such as quinine, is consumed and binds to G protein-coupled receptors.II. Part II is the transduction pathway 2. Gustducin, a G protein second messenger, is activated. 3. Phosphodiesterase, an enzyme, is then activated. 4. Cyclic nucleotide, cNMP, is used, lowering the concentration 5. Channels such as the K+, potassium, channels, close. III. Part III is the response of the taste cell. 6. This leads to increased levels of Ca+. 7. The neurotransmitters are activated. 8. The signal is sent to the neuron.
Bitterness is of interest to those who studyevolution, as well as various health researchers[24][32] since a large number of natural bitter compounds are known to be toxic. The ability to detect bitter-tasting, toxic compounds at low thresholds is considered to provide an important protective function.[24][32][33] Plant leaves often contain toxic compounds, and amongleaf-eating primates there is a tendency to prefer immature leaves, which tend to be higher in protein and lower in fiber and poisons than mature leaves.[34] Amongst humans, variousfood processing techniques are used worldwide to detoxify otherwise inedible foods and make them palatable.[35] Furthermore, the use of fire, changes in diet, and avoidance of toxins has led to neutral evolution in human bitter sensitivity. This has allowed several loss of function mutations that has led to a reduced sensory capacity towards bitterness in humans when compared to other species.[36]
The threshold for stimulation of bitter taste by quinine averages a concentration of 8 μM (8 micromolar).[24] The taste thresholds of other bitter substances are rated relative to quinine, which is thus given a reference index of 1.[24][25] For example,brucine has an index of 11, is thus perceived as intensely more bitter than quinine, and is detected at a much lower solution threshold.[24] The most bitter natural substance isamarogentin, a compound present in the roots of the plantGentiana lutea, and the most bitter substance known is the synthetic chemicaldenatonium, which has an index of 1,000.[25] It is used as anaversive agent (abitterant) that is added to toxic substances to prevent accidental ingestion. It was discovered accidentally in 1958 during research on a local anesthetic byT. & H. Smith ofEdinburgh, Scotland.[37][38]
Research has shown that TAS2Rs (taste receptors, type 2, also known as T2Rs) such asTAS2R38 coupled to theG proteingustducin are responsible for the human ability to taste bitter substances.[39] They are identified not only by their ability to taste for certain "bitter"ligands, but also by the morphology of the receptor itself (surface bound, monomeric).[18] The TAS2R family in humans is thought to comprise about 25 different taste receptors, some of which can recognize a wide variety of bitter-tasting compounds.[40] Over 670 bitter-tasting compounds have been identified, on abitter database, of which over 200 have been assigned to one or more specific receptors.[41] It is speculated that the selective constraints on the TAS2R family have been weakened due to the relatively high rate of mutation and pseudogenization.[42] Researchers use two synthetic substances,phenylthiocarbamide (PTC) and6-n-propylthiouracil (PROP) to study thegenetics of bitter perception. These two substances taste bitter to some people, but are virtually tasteless to others. Among the tasters, some are so-called "supertasters" to whom PTC and PROP are extremely bitter. The variation in sensitivity is determined by two common alleles at the TAS2R38 locus.[43] This genetic variation in the ability to taste a substance has been a source of great interest to those who study genetics.
Gustducin is made of three subunits. When it is activated by the GPCR, its subunits break apart and activatephosphodiesterase, a nearby enzyme, which in turn converts a precursor within the cell into a secondary messenger, which closes potassium ion channels.[citation needed] Also, this secondary messenger can stimulate theendoplasmic reticulum to release Ca2+ which contributes to depolarization. This leads to a build-up of potassium ions in the cell, depolarization, and neurotransmitter release. It is also possible for some bitter tastants to interact directly with the G protein, because of a structural similarity to the relevant GPCR.
The most bitter substance known to date –oligoporin D – stimulates the bitter taste receptor type TAS2R46 at the lowest concentrations 100 nM (0.1 micromolar, approx. 63 millionths of a gram/liter).[44][45]
Umami was first studied in 1907 byIkeda isolatingdashi taste, which he identified as the chemicalmonosodium glutamate (MSG).[17][51] MSG is a sodium salt that produces a strong savory taste, especially combined with foods rich innucleotides such as meats, fish, nuts, and mushrooms.[52]
Some savory taste buds respond specifically to glutamate in the same way that "sweet" ones respond to sugar. Glutamate binds to a variant ofG protein coupled glutamate receptors.[53][54] L-glutamate may bond to a type of GPCR known as a metabotropic glutamate receptor (mGluR4) which causes the G-protein complex to activate the sensation of umami.[54]
Perceptual independence from salty and sweet taste
There are doubts regarding whether umami is different from salty taste, as standalone glutamate(glutamic acid) without table salt ions(Na+), is perceived as sour, salt taste blockers reduce discrimination between monosodium glutamate and sucrose in rodents, since sweet and umami tastes share a taste receptor subunit; and part of the human population cannot tell apart umami from salty.[55]
If umami doesn't have perceptual independence, it could be classified with other tastes like fat, carbohydrate, metallic, and calcium, which can be perceived at high concentrations but may not offer a prominent taste experience.[56]
Measuring the degree to which a substance presents one basic taste can be achieved in a subjective way by comparing its taste to a reference substance.
Sweetness is subjectively measured by comparing the threshold values, or level at which the presence of a dilute substance can be detected by a human taster, of different sweet substances.[57] Substances are usually measured relative tosucrose,[58] which is usually given an arbitrary index of 1[59][60] or 100.[61]Rebaudioside A is 100 times sweeter than sucrose;fructose is about 1.4 times sweeter;glucose, a sugar found in honey and vegetables, is about three-quarters as sweet; andlactose, a milk sugar, is one-half as sweet.[b][57]
The sourness of a substance can be rated by comparing it to very dilutehydrochloric acid (HCl).[62]
Relative saltiness can be rated by comparison to a dilute salt solution.[63]
Quinine, a bitter medicinal found intonic water, can be used to subjectively rate the bitterness of a substance.[64] Units of dilute quinine hydrochloride (1 g in 2000 mL of water) can be used to measure the threshold bitterness concentration, the level at which the presence of a dilute bitter substance can be detected by a human taster, of other compounds.[64] More formal chemical analysis, while possible, is difficult.[64]
There may not be an absolute measure for pungency, though there are tests for measuring the subjective presence of a given pungent substance in food, such as theScoville scale for capsaicine in peppers or thePyruvate scale forpyruvates in garlics and onions.
Taste buds and papillae of the human tongueTaste receptors of the human tongueSignal transduction of taste receptors
Taste is a form ofchemoreception which occurs in the specialisedtaste receptors in the mouth. To date, there are five different types of taste these receptors can detect which are recognized: salt, sweet, sour, bitter, and umami. Each type of receptor has a different manner ofsensory transduction: that is, of detecting the presence of a certain compound and starting an action potential which alerts the brain. It is a matter of debate whether each taste cell is tuned to one specific tastant or to several; Smith and Margolskee claim that "gustatory neurons typically respond to more than one kind of stimulus, [a]lthough each neuron responds most strongly to one tastant". Researchers believe that the brain interprets complex tastes by examining patterns from a large set of neuron responses. This enables the body to make "keep or spit out" decisions when there is more than one tastant present. "No single neuron type alone is capable of discriminating among stimuli or different qualities, because a given cell can respond the same way to disparate stimuli."[65] As well,serotonin is thought to act as an intermediary hormone which communicates with taste cells within a taste bud, mediating the signals being sent to the brain. Receptor molecules are found on the top ofmicrovilli of the taste cells.
Sweetness is produced by the presence ofsugars, some proteins, and other substances such as alcohols likeanethol,glycerol andpropylene glycol,saponins such asglycyrrhizin,artificial sweeteners (organic compounds with a variety of structures), andlead compounds such aslead acetate.[citation needed] It is often connected toaldehydes andketones, which contain acarbonyl group.[citation needed] Many foods can be perceived as sweet regardless of their actual sugar content. For example, some plants such asliquorice,anise orstevia can be used as sweeteners.Rebaudioside A is asteviol glycoside coming from stevia that is 200 times sweeter than sugar. Lead acetate and other lead compounds were used as sweeteners, mostly for wine, untillead poisoning became known. Romans used to deliberately boil the must inside of lead vessels to make a sweeter wine.Sweetness is detected by a variety ofG protein-coupled receptors coupled to aG protein that acts as an intermediary in the communication between taste bud and brain,gustducin.[66] These receptors are T1R2+3 (heterodimer) and T1R3 (homodimer), which account for sweet sensing in humans and other animals.[67]
Saltiness is a taste produced best by the presence ofcations (such asNa+ ,K+ orLi+ )[68] and is directly detected by cation influx into glial like cells via leak channels causing depolarisation of the cell.[68]
Sourness isacidity,[69][70] and, like salt, it is a taste sensed usingion channels.[68] Undissociated acid diffuses across the plasma membrane of a presynaptic cell, where it dissociates in accordance withLe Chatelier's principle. The protons that are released then block potassium channels, which depolarise the cell and cause calcium influx. In addition, the taste receptor PKD2L1 has been found to be involved in tasting sour.[71]
Research has shown that TAS2Rs (taste receptors, type 2, also known as T2Rs) such asTAS2R38 are responsible for the ability to taste bitter substances in vertebrates.[72] They are identified not only by their ability to taste certain bitter ligands, but also by the morphology of the receptor itself (surface bound, monomeric).[73]
The tongue can also feel other sensations not generally included in the basic tastes. These are largely detected by thesomatosensory system. In humans, the sense of taste is conveyed via three of the twelve cranial nerves. Thefacial nerve (VII) carries taste sensations from the anterior two thirds of thetongue, theglossopharyngeal nerve (IX) carries taste sensations from the posterior one third of the tongue while a branch of thevagus nerve (X) carries some taste sensations from the back of the oral cavity.
Thetrigeminal nerve (cranial nerve V) provides information concerning the general texture of food as well as the taste-related sensations of peppery or hot (fromspices).
This particular sensation, calledchemesthesis, is not a taste in the technical sense, because the sensation does not arise from taste buds, and a different set of nerve fibers carry it to the brain. Foods like chili peppers activate nerve fibers directly; the sensation interpreted as "hot" results from the stimulation of somatosensory (pain/temperature) fibers on the tongue. Many parts of the body with exposed membranes but no taste sensors (such as the nasal cavity, under the fingernails,surface of the eye or a wound) produce a similar sensation of heat when exposed to hotness agents.
Some substances activate coldtrigeminal receptors even when not at low temperatures. This "fresh" or "minty" sensation can be tasted inpeppermint andspearmint and is triggered by substances such asmenthol,anethol, ethanol, andcamphor. Caused by activation of the same mechanism that signals cold,TRPM8 ion channels onnerve cells, unlike the actual change in temperature described for sugar substitutes, this coolness is only a perceived phenomenon.
Both Chinese andBatak Toba cooking include the idea of 麻 (má) ormati rasa, a tingling numbness caused by spices such asSichuan pepper. The cuisines ofSichuan province in China and of the Indonesian province ofNorth Sumatra often combine this withchili pepper to produce a 麻辣málà, "numbing-and-hot", or "mati rasa" flavor.[77]Typical in northern Brazilian cuisine,jambu is an herb used in dishes liketacacá.These sensations, although not taste, fall into a category ofchemesthesis.
Some foods, such as unripe fruits, containtannins orcalcium oxalate that cause an astringent or puckering sensation of the mucous membrane of the mouth. Examples includetea,red wine, orrhubarb.[citation needed] Other terms for the astringent sensation are "dry", "rough", "harsh" (especially for wine), "tart" (normally referring to sourness), "rubbery", "hard" or "styptic".[78]
A metallic taste may be caused by food and drink, certain medicines oramalgam dental fillings. It is generally considered an off flavor when present in food and drink. A metallic taste may be caused bygalvanic reactions in the mouth. In the case where it is caused by dental work, the dissimilar metals used may produce a measurable current.[79] Some artificial sweeteners are perceived to have a metallic taste, which is detected by theTRPV1 receptors.[80] Many people considerblood to have a metallic taste.[81][82] A metallic taste in the mouth is also a symptom of various medical conditions, in which case it may be classified under the symptomsdysgeusia orparageusia, referring to distortions of the sense of taste,[83] and can be caused by medication, includingsaquinavir,[83]zonisamide,[84] and various kinds ofchemotherapy,[85] as well as occupational hazards, such as working withpesticides.[86]
Recent research reveals a potentialtaste receptor called theCD36 receptor.[87][88][89] CD36 was targeted as a possible lipid taste receptor because it binds tofat molecules (more specifically, long-chainfatty acids),[90] and it has been localized totaste bud cells (specifically, the circumvallate and foliatepapillae).[91] There is a debate over whether we can truly taste fats, and supporters of human ability to taste free fatty acids (FFAs) have based the argument on a few main points: there is an evolutionary advantage to oral fat detection; a potential fat receptor has been located on taste bud cells; fatty acids evoke specific responses that activategustatory neurons, similar to other currently accepted tastes; and, there is a physiological response to the presence of oral fat.[92] Although CD36 has been studied primarily inmice, research examining human subjects' ability to taste fats found that those with high levels of CD36expression were more sensitive to tasting fat than were those with low levels of CD36 expression;[93] this study points to a clear association between CD36 receptor quantity and the ability to taste fat.
Monovalent cation channelTRPM5 has been implicated in fat taste as well,[96] but it is thought to be involved primarily in downstream processing of the taste rather than primary reception, as it is with other tastes such as bitter, sweet, and savory.[92]
Proposed alternate names to fat taste include oleogustus[97] and pinguis,[22] although these terms are not widely accepted. The main form of fat that is commonly ingested istriglycerides, which are composed of three fatty acids bound together. In this state, triglycerides are able to give fatty foods unique textures that are often described as creaminess. But this texture is not an actual taste. It is only during ingestion that the fatty acids that make up triglycerides are hydrolysed into fatty acids via lipases. The taste is commonly related to other, more negative, tastes such as bitter and sour due to how unpleasant the taste is for humans. Richard Mattes, a co-author of the study, explained that low concentrations of these fatty acids can create an overall better flavor in a food, much like how small uses of bitterness can make certain foods more rounded. A high concentration of fatty acids in certain foods is generally considered inedible.[98] To demonstrate that individuals can distinguish fat taste from other tastes, the researchers separated volunteers into groups and had them try samples that also contained the other basic tastes. Volunteers were able to separate the taste of fatty acids into their own category, with some overlap with savory samples, which the researchers hypothesized was due to poor familiarity with both. The researchers note that the usual "creaminess and viscosity we associate with fatty foods is largely due to triglycerides", unrelated to the taste; while the actual taste offatty acids is not pleasant. Mattes described the taste as "more of a warning system" that a certain food should not be eaten.[99]
There are few regularly consumed foods rich in fat taste, due to the negative flavor that is evoked in large quantities. Foods whose flavor to which fat taste makes a small contribution include olive oil and fresh butter, along with various kinds of vegetable and nut oils.[100]
Kokumi (/koʊkuːmi/, Japanese:kokumi (コク味)[101] fromkoku (こく)[101]) is translated as "heartiness", "full flavor" or "rich" and describes compounds in food that do not have their own taste, but enhance the characteristics when combined.
Alongside the five basic tastes of sweet, sour, salt, bitter and savory,kokumi has been described as something that may enhance the other five tastes by magnifying and lengthening the other tastes, or "mouthfulness".[102]: 290 [103] Garlic is a common ingredient to add flavor used to help define the characteristickokumi flavors.[103]
Calcium-sensing receptors (CaSR) are receptors forkokumi substances which, applied around taste pores, induce an increase in the intracellular Ca concentration in a subset of cells.[102] This subset of CaSR-expressing taste cells are independent from the influenced basic taste receptor cells.[104] CaSR agonists directly activate the CaSR on the surface of taste cells and integrated in the brain via the central nervous system. A basal level of calcium, corresponding to the physiological concentration, is necessary for activation of the CaSR to develop thekokumi sensation.[105]
The distinctive taste of chalk has been identified as the calcium component of that substance.[106] In 2008, geneticists discovered acalcium receptor on the tongues ofmice. The CaSR receptor is commonly found in thegastrointestinal tract,kidneys, andbrain. Along with the "sweet" T1R3 receptor, the CaSR receptor can detect calcium as a taste. Whether the perception exists or not in humans is unknown.[107][108]
Temperature can be an essential element of the taste experience. Heat can accentuate some flavors and decrease others by varying the density and phase equilibrium of a substance. Food and drink that—in a given culture—is traditionally served hot is often considered distasteful if cold, and vice versa. For example, alcoholic beverages, with a few exceptions, are usually thought best when served at room temperature or chilled to varying degrees, but soups—again, with exceptions—are usually only eaten hot. A cultural example aresoft drinks. In North America it is almost always preferred cold, regardless of season.
A 2016 study suggested that humans can tastestarch (specifically, aglucoseoligomer) independently of other tastes such as sweetness, without suggesting an associated chemical receptor.[109][110][111]
Active brain areas in taste perceptionThis diagram linearly (unless otherwise mentioned) tracks the projections of all known structures that allow for taste to their relevant endpoints in the human brain.
The lingual nerve (trigeminal, not shown in diagram) is deeply interconnected with the chorda tympani in that it provides all other sensory info from the anterior two-thirds of the tongue.[113] This info is processed separately (nearby) in the rostral lateral subdivision of the nucleus of the solitary tract (NST).
The NST receives input from the amygdala (regulates oculomotor nuclei output),bed nuclei of stria terminalis, hypothalamus, and prefrontal cortex. The NST is the topographical map that processes gustatory and sensory (temp, texture, etc.) info.[114]
The reticular formation (includes Raphe nuclei responsible for serotonin production) is signaled to release serotonin during and after a meal to suppress appetite.[115] Similarly, salivary nuclei are signaled to decrease saliva secretion.
Insects taste using small hair-like structures called taste sensilla, specialized sensory organs located on various body parts such as the mouthparts, legs, and wings. These sensilla contain gustatory receptor neurons (GRNs) sensitive to a wide range of chemical stimuli.
Insects respond to sugar, bitter, acid, and salt tastes. However, their taste spectrum extends to include water, fatty acids, metals, carbonation, RNA, ATP, and pheromones. Detecting these substances is vital for behaviors like feeding, mating, and oviposition.
Invertebrates' ability to taste these compounds is fundamental to their survival and provides insights into the evolution of sensory systems. This knowledge is crucial for understanding insect behavior and has applications in pest control and pollination biology.
A supertaster is a person whose sense of taste is significantly more sensitive than most. The cause of this heightened response is likely, at least in part, due to an increased number offungiform papillae.[119] Studies have shown that supertasters require less fat and sugar in their food to get the same satisfying effects. These people tend to consume more salt than others. This is due to their heightened sense of the taste of bitterness, and the presence of salt drowns out the taste of bitterness.[120]
Aftertastes arise after food has been swallowed. An aftertaste can differ from the food it follows.Medicines and tablets may also have a lingering aftertaste, as they can contain certain artificial flavor compounds, such asaspartame (artificial sweetener).
An acquired taste often refers to an appreciation for a food or beverage that is unlikely to be enjoyed by a person who has not had substantial exposure to it, usually because of some unfamiliar aspect of the food or beverage, including bitterness, a strong or strange odor, taste, or appearance.
Inthe West,Aristotle postulated inc. 350BC[124] that the two most basic tastes were sweet and bitter.[125] He was one of the first persons to develop a list of basic tastes.[126]
Thereceptors for the basic tastes of bitter, sweet and savory have been identified. They areG protein-coupled receptors.[127] The cells that detect sourness have been identified as a subpopulation that express the proteinPKD2L1, and The responses are mediated by an influx of protons into the cells.[127] As of 2019, molecular mechanisms for each taste appear to be different, although all taste perception relies on activation ofP2X purinoreceptors onsensory nerves.[128]
a.^ It has been known for some time that these categories may not be comprehensive. In Guyton's 1976 edition ofTextbook of Medical Physiology, he wrote:
On the basis of physiologic studies, there are generally believed to be at least fourprimary sensations of taste:sour,salty,sweet, andbitter. Yet we know that a person can perceive literally hundreds of different tastes. These are all supposed to be combinations of the four primary sensations...However, there might be other less conspicuous classes or subclasses of primary sensations",[129]
b.^ Some variation in values is not uncommon between various studies. Such variations may arise from a range of methodological variables, from sampling to analysis and interpretation. In fact there is a "plethora of methods"[130] Indeed, the taste index of 1, assigned to reference substances such as sucrose (for sweetness), hydrochloric acid (for sourness), quinine (for bitterness), and sodium chloride (for saltiness), is itself arbitrary for practical purposes.[62]
Some values, such as those for maltose and glucose, vary little. Others, such as aspartame and sodium saccharin, have much larger variation. Regardless of variation, the perceived intensity of substances relative to each reference substance remains consistent for taste ranking purposes. The indices table for McLaughlin & Margolskee (1994) for example,[24][25] is essentially the same as that of Svrivastava & Rastogi (2003),[131] Guyton & Hall (2006),[62] and Joestenet al. (2007).[59] The rankings are all the same, with any differences, where they exist, being in the values assigned from the studies from which they derive.
As for the assignment of 1 or 100 to the index substances, this makes no difference to the rankings themselves, only to whether the values are displayed as whole numbers or decimal points. Glucose remains about three-quarters as sweet as sucrose whether displayed as 75 or 0.75.
^abBoron, W.F., E.L. Boulpaep. 2003. Medical Physiology. 1st ed. Elsevier Science USA.
^Kean, Sam (Fall 2015)."The science of satisfaction".Distillations Magazine.1 (3): 5.Archived from the original on 17 November 2019. Retrieved20 March 2018.
^Scinska A, Koros E, Habrat B, Kukwa A, Kostowski W, Bienkowski P (August 2000). "Bitter and sweet components of ethanol taste in humans".Drug and Alcohol Dependence.60 (2):199–206.doi:10.1016/S0376-8716(99)00149-0.PMID10940547.
^Jones, S., Martin, R., & Pilbeam, D. (1994)The Cambridge Encyclopedia of Human Evolution. Cambridge: Cambridge University Press[page needed]
^Johns, Timothy (1990).With Bitter Herbs They Shall Eat It: Chemical ecology and the origins of human diet and medicine. Tucson: University of Arizona Press.ISBN0816510237.[page needed]
^abcChaudhari N, Landin AM, Roper SD (February 2000). "A metabotropic glutamate receptor variant functions as a taste receptor".Nature Neuroscience.3 (2):113–9.doi:10.1038/72053.PMID10649565.S2CID16650588.
^Walters, D. Eric (13 May 2008),"How is Sweetness Measured?",All About Sweeteners,archived from the original on 24 December 2010, retrieved15 September 2010
^abcGuyton, Arthur C; Hall, John E. (2006),Guyton and Hall Textbook of Medical Physiology (11th ed.), Philadelphia: Elsevier Saunders, p. 664,ISBN978-0-7216-0240-0
^Simons, P. J.; Kummer, J. A.; Luiken, J. J.; Boon, L (2011). "Apical CD36 immunolocalization in human and porcine taste buds from circumvallate and foliate papillae".Acta Histochemica.113 (8):839–43.doi:10.1016/j.acthis.2010.08.006.PMID20950842.
^Eliav, Eli, and Batya Kamran. "Evidence of Chorda Tympani Dysfunction in Patients with Burning Mouth Syndrome."Science Direct. May 2007. Web. 27 March 2016.
^Mu, Liancai, and Ira Sanders. "Human Tongue Neuroanatomy: Nerve Supply and Motor Endplates." Wiley Online Library. Oct. 2010. Web. 27 March 2016.
^King, Camillae T., and Susan P. Travers. "Glossopharyngeal Nerve Transection Eliminates Quinine-Stimulated Fos-Like Immunoreactivity in the Nucleus of the Solitary Tract: Implications for a Functional Topography of Gustatory Nerve Input in Rats." JNeurosci. 15 April 1999. Web. 27 March 2016.
^Hornung, Jean-Pierre. "The Human Raphe Nuclei and the Serotonergic System."Science Direct. Dec. 2003. Web. 27 March 2016.
^Reiner, Anton, and Harvey J. Karten. "Parasympathetic Ocular Control — Functional Subdivisions and Circuitry of the Avian Nucleus of Edinger-Westphal."Science Direct. 1983. Web. 27 March 2016.
^Wright, Christopher I., and Brain Martis. "Novelty Responses and Differential Effects of Order in the Amygdala, Substantia Innominata, and Inferior Temporal Cortex." Science Direct. Mar. 2003. Web. 27 March 2016.
^Menon, Vinod, and Lucina Q. Uddin. "Saliency, Switching, Attention and Control: A Network Model of Insula." Springer. 29 May 2010. Web. 28 March 2016.
