Who Tastes Best?

Biology concepts – taste/gustation, aposematism, carnivore, herbivore, omnivore, Jacobson’s organ, palatal organ, parasite

What animal do you think has the most taste buds? There are bunches of animals out there, so let’s make it a bit easier. What sorts of animals do you think would need more taste buds? Omnivores might be a good choice, since they eat more different kinds of foods.

Cows are big, so they have big tongues. It isn’t too surprising

that they have many taste buds. However, the density (number

per unit area) is higher than most animals too, since they eat

plants, and they have to pick the non-poisonous plants from the

poisonous. Some people eat beef tongue – Bill Cosby said he

didn’t want to taste anything that might taste him back. I would

add that I don’t want to eat anything that could have been

in a cow’s nose.

Carnivores could be a choice, since they have to worry (most of them, vultures excepted) about rotted or diseased meat. But then again, herbivores might be the answer; they eat plants, and plants are the source of most poisons. The same could be said about insectivores, the insects they eat are often toxic – formic acid in ants or stored plant toxins.

Let’s take a survey of animals and see if a pattern develops. Humans have about 10,000 taste buds on average. Young people have more than the elderly; you lose about half your taste buds by age 65. Women generally have more than men. And supertasters can have double the number of non-tasters. But 10,000 is a good number to go by.

Pigs have about 15,000 taste buds while cows have 25,000 and rabbits average 17,000. Lions and other cats come in at about 450 taste buds, but dogs fair better, averaging about 1200. Birds have very few and some fish have alot, but we will talk about them below.

Sort the numbers out and it appears that herbivores have the highest number of taste buds, carnivores and insectivores the fewest, and omnivores lie somewhere in the middle. It looks like keeping an eye (or tongue) out for poisonous plants is the most important mechanism for taste. Carnivores’ strict diet means they need fewer, as we saw when we discussed the loss of sweet taste receptors in cats.

But the winner in the taste bud count? Believe it or not – catfish! Even small catfish (6 in/15 cm) have about 250,000 taste buds. They are literally covered in taste buds. Mind you, we’re talking about taste buds, not just taste receptor cells like we discussed last week. These are full-fledged taste buds, with at least five different tastes represented (sweet, salt, bitter, sour, umami).

On this light colored fish skin, you can see the dots that

are the microscopic taste buds. I eat fish skin, but I don’t

equate it to eating cow tongue.

Most fish have the majority of their taste buds in their mouths - that makes sense. Some fish, especially bottom feeders like carp, are designed so that food coming into contact with the back of the roof the mouth will stimulate an area called the palatal organ which has thousands of taste buds. When the muscular palatal organ tastes food, it automatically clamps down on the food particle. Everything else - water, stones, inedible things - are then flushed from the mouth by blowing them out. Only the food is left and they swallow it.

That’s pretty much it for fish with scales, but catfish, sharks, and some other fish don’t have scales, they are covered with tissue that is more like skin. In these kinds of fishes, it’s like their tongues have migrated all over their bodies. They taste with everything – mouth, lips, gills, fins, body, tail, whiskers.

The catfish, as ironic as it may be, doesn’t have taste buds on its tongue! Why would it be important for catfish to have so many taste buds but none on their tongues? It’s because they live in muddy water. Their sight is impaired, so the taste buds on their body allow them to find food. In truth, most fish have very few taste buds on their tongue (called a basihyal amongst ichthyologists). 

This is fortuitous for a fish parasite called Cymothoa exigua. It may sound disgusting, but this isopod (iso = identical, and pod = foot) parasite makes its living by getting into a fish’s mouth through its gills, eating its tongue and then replacing the missing tongue with its own body. Now, everything that comes into the fish’s mouth can be nibbled on by the parasite.

C. exigua doesn’t so much eat its host’s tongue as it causes it to disappear. It grabs on to the tongue, and sucks the blood out of it. The longer this goes on, the more the tongue atrophies (a = no, and trophic = feeding) and shrinks away to nothing. Then the parasite grabs hold of the stump with its back legs and takes its place.

An amazing picture of the isopod parasite C. exigua acting

as the tongue of a captured fish. It lives in the gulf of

California and usually selects the rose snapper as a host.

Every once in a while, a fish lands in the grocery store

with a parasite still hanging on, looking for the next meal.

I’m guessing that fish gets returned and a lot of store

credit is issued. Photo credit to Dr. Nico Smit.

Talk about exceptional; this is the only known instance where a parasite functionally replaces a host’s own organ. The isopod is willing to act like a tongue, holding food up against the small teeth on the roof of the fish’s mouth, because this is how it ensures food for itself.

We know that taste is important for animals to separate toxins from those foods that are good for them, so it is probably fortunate that fish don’t use their tongue for tasting. If losing their tongue caused fish to die more often from ingested poisons or from starvation, then the parasite would be sealing its own fate – it wants its host to survive.

Moving on to something a little less disgusting. We talkedlast week about solitary chemosensory cells and their work in non-gustatory organs. An interesting 2013 paper studied the SCC and taste buds of fish and compared them to those of mammals. Their results indicate that taste buds did not evolve from SCCs or vice versa, the two developed independently. This means that taste, smell and nutrient sensing all developed on their own, yet they have similar and overlapping structures and functions. A good smell idea is a good taste idea.

Snakes show again the similarities between taste and smell. Most snakes (some sea snakes excepted) have taste buds, often lined up near their teeth. What is different is the vomeronasal organ (Jacobson’s organ) for sensing volatile chemicals. Present in amphibians, most reptiles (not crocodiles or chameleons), and some mammals, the VNO is for sensing pheromones and other scents.

On the left is a cartoon showing the snake veromonasal organ

(VNO). It sits in the roof of the mouth and neurons from it go

to the olfactory bulb. As the tongue pulls in molecules, it

presses the tongue up into the VNO. On the top right, you see

how the snake spreads its tongue out to pick up as many signals

as possible. Now you know why snakes have forked tongues.

On the bottom right, you see that the VNO doesn’t even

communicate directly with the nostrils, the moth is more

important for this smelling.

In snakes, however, the scents are not brought to the organ by breathing in. In fact, the VNO in snakes isn’t even open to the nasal compartment. Instead, snakes bring the scent molecules in with their tongue, and press them into the VNO for sensing. This makes it a quasi-direct chemosensory organ, like taste. And thus, we run up against the crossover of smell and taste again.

Humans can taste some volatile compounds as well. One nasty example is gasoline. If confronted with gasoline fumes in sufficient density, some will enter your mouth and mix with saliva. If enough molecules come into contact with your taste buds, you will taste the gas – not an especially pleasant taste.

Even more exceptional, you can also taste a gas you didn’t breathe in. There is a chemical called dimethyl sulfoxide (DMSO) that is used in many laboratories. It’s famous for being a great solvent. A solvent is a liquid in which other chemicals will dissolve. Water is a very good solvent, but there are many things that are not water-soluble.

Once inside the body, DMSO starts to be metabolized by your cells. One of the products of its breakdown is dimethyl sulfide (DMS). This travels around in your blood, but wants to a gas, so it passes from your blood to your lungs. From here you breathe it out. When you exhale DMS, you taste it. It tastes and smells like garlic, so if you taste this and haven’t had Italian for lunch, then you might have contaminated yourself with DMSO - oops.

DMSO is a by product of the wood industry and is a great

solvent. It is polar solvent, meaning that it has a partial

positive charge and a partial negative charge within its

structure. Scientists first thought that the sulfur (S) oxygen

(O) bond was a double bond, but it turns out to be a single

bond with the excess charge being shared as a huge dipole.

Being so much more polar makes it a great solvent, it can get

in between nonpolar, positive or negative structures to

help things dissolve.

The oops is because the structure of DMSO allows almost anything to go into solution – it would put your car into solution if you have enough of it. Its structure also makes it so DMSO can be absorbed directly through your skin to your bloodstream. Any molecule dissolved in DMSO will also be carried straight into your tissues.

This works out well for medicine and chemistry, as certain tests or drugs require that the chemical be dissolved. But, if you happen to be using a toxic chemical in DMSO and get some of it on your skin or mucous membranes - you’ve now been poisoned and you just hope it wasn’t enough to kill you.

Back to taste buds. At the low end of the taste bud spectrum are the birds. They have merely dozens (Japanese quail) to a couple hundred taste buds; chickens and songbirds are especially taste-poor. But that doesn’t mean they can’t be interesting. In the 1970’s, it was discovered that ducks had taste buds in a weird place – on their beaks.

Mallard ducks therefore have about 400 taste buds on their jaws, since beak parts are extensions of the maxilla (upper jaw) and mandible (lower jaw) bones. The taste buds are located in five concentrations, four on the maxilla and one on the mandible.

These positions just happen to correspond to where the duck grasps and holds food as it decides whether it is safe to swallow. Once again, life is protected by taste sense.

The leopard lacewing caterpillar on the left warns predators

with its bright colors that it is poisonous. This is

aposematism, although some animals aren’t above

faking that they are poisonous by just adopting the colors.

On the right is the crimson speckled moth, it is bright and

patterned, but it does it for a different reason. This is a

secondary sex characteristic for attracting mates.

So birds can taste their food, but they don’t rely just on that. It was back in Darwin’s day that the question was raised as to why birds would eat green and brown caterpillars but leave bright colored caterpillars alone. This led Alfred Russel Wallace (the other guy who came up with natural selection) to demonstrate the concept of aposematism (apo = away, and semantic = sign), coloration to warn of toxicity in order to ward off predation.

The bright color says, “Don’t eat me, I’m poisonous.” This is important because even a single peck with a beak could be lethal to a caterpillar. Birds learned quickly to avoid the bright caterpillars, suggesting that birds could taste. This tale is well recounted in the 2012 book of Tim Birkhead, called Bird Sense.

In a strange twist, there are a few birds that are toxic because of their diet, the pithoui and the ifrita. We have discussed these birds in terms of toxins. These birds are brightly colored, so they are using the concept of aposematism to keep themselves safe, just like many potential bird snacks do.

Speaking of caterpillars, we’ll get to arthropod gustatory sense next week. It turns out that some insects taste with their wings, while others taste different things based on their jobs.

Kirino M, Parnes J, Hansen A, Kiyohara S, & Finger TE (2013). Evolutionary origins of taste buds: phylogenetic analysis of purinergic neurotransmission in epithelial chemosensors. Open biology, 3 (3) PMID: 23466675

Tim Birkhead (2012). Bird Sense: What It Is Like To Be Bird Walker Publishing, New York

For more information, see:

Cymothoa exigua –

http://www.wired.com/wiredscience/2013/11/absurd-creature-of-the-week-the-parasite-that-eats-and-replaces-a-fishs-tongue/

http://phenomena.nationalgeographic.com/2013/02/28/tongue-eating-fish-parasites-never-cease-to-amaze/

http://www.talksciencetome.com/treasures-the-tongue-eating-sea-louse/

Tasting With Every Part Of Your Body

Biology concepts – taste sensation, non-lingual taste receptors, solitary chemoreceptor cells

Bitter melon (Momordica charantia) goes by many names,

like goya, kalera, etc. It is native to the subcontinent and Asia,

and is used in many cuisines. I have not tried it, but I have

heard it described as tasting like evil, or a cross between

uncooked collard greens and chewing on aspirin. Despite this,

there is a bittermelon soda sold in Japan. My point – even

though bitter is supposed to warn of poison, people can learn

to love it. Are they more likely to be poisoned?

In our recent discussions of the gustatory sense (here, here, and here), we have highlighted the idea that taste is basically a nutrient/poison detection system. You can avoid toxins (sour, bitter) or find nutrients (salty, sweet, umami, fat) of based just on taste. In terms of avoiding toxins; you taste it, and hopefully don’t swallow enough to be harmful to you.

A question occurs to me in this scenario – why not taste things somewhere other than the opening of your gastrointestinal (GI) system? You would be much less likely to ingest a toxin if you never put it in your mouth. Tasting something with the ends of your fingers, for example, would identify sour and bitter – things to toss toward your enemy, and could identify cupcakes and filet mignon as well. Everything would be finger food.

Yet there they are, all those taste buds sitting on our tongue, the inviting front porch swing to our GI tract. Frogs, civet cats, owls – vertebrates of all types have oral taste buds. But it gets weird if you want to start counting all of them, because they aren’t all on your tongue. There are taste buds on your palate (roof of your mouth) and in your throat, and these are just the taste buds. It gets weirder - animals have taste cells and taste receptors in some really weird places.

We have discussed, and will discuss again, how closely related are smell and taste, how they work on a molecular level and how the senses work together to form a flavor. We know now that mammals have taste receptors in their noses!

Bitter taste receptor cells are scattered throughout the nasal cavity, not grouped together in taste buds, so they are called solitary chemoreceptor cells. Maybe this is a way to detect bitter and possibly toxic stimuli before you put them in your mouth - our idea of evolving protective taste sense outside the GI tract may not be some dumb after all. However, the original paper saw that they were linked to increasing respiration rate (to get toxic substances out of the lungs faster).

Here is most of your gastrointestinal tract. The elements

underlined in red have been shown to express taste

receptors. They may acts as nutrient sensors, as hunger

modulators, or even protection against poisoning. To

understand what those mean – read the post! Those not

underlined most likely express the receptors too, they

just haven’t been studied for that yet.

The GI system happens to have many taste receptors; the stomach, small bowel, and large bowel (colon) of mammals have receptors for sweet, fat, bitter, and umami. Interesting that these are the receptors for nutrients and toxins. If you happen to swallow a bitter toxin, the gut receptors stimulate an ion release into the gut.

Water follows the ions due to osmotic pressure, and this would help to flush the toxin through the system faster (ie. diarrhea). This makes sense, but I don’t know if it plays out that way in real life. Not everybody gets to spend hours in the bathroom after eating something bitter - there are probably other issues in play.

On a sweeter note, it has been shown that many intestinal cells express functional sweet heterodimer receptors (T1R2 + T1R3). Cells call enteroendocrine cells (entero = gut, endo = within, and crine = distinguish) produce many of these receptors, and act as sensors for sugar in the gut.

When the enteroendocrine cells detect sugar or artificial sweeteners, they produce hormones that stimulate other gut cells to make more glucose transporters. This is another way that your body works hard to make sure you get all the carbohydrate you can for energy production – it never wants a carbohydrate to get through the gut without being snatched up for use.

Umami receptors are also found in the gut, including the enteroendocrine cells. It was shown in 2013 (here and here) that amino acids are sensed by these receptors, and stimulate release of a hormone called cholecystokinin (CCK), which works in part to tell your brain you that are full.

Cholecystokinin (CCK) is a multifunctional hormone

released from the small intestine after consuming proteins

or fats. It is a hunger suppressant; appetite is controlled by

the hypothalamus of the brain. It can’t cross the blood brain

barrier (BBB), but the hypothalamus isn’t protected by the

BBB. Interesting, no? It just happens that CCK is inhibited

by capsaicin, so maybe it isn’t a good idea to eat spicy and

fatty foods in the same sitting.

CCK also stimulates the release of bile from the gall bladder to aid in the digestion of fats. Fats and amino acids go hand in hand, since meat contains much of both. This may account for the presence of fat taste receptors (CD36 and GPR120) in the gut as well. Fat is harder to digest that other nutrients, so CCK stimulates a slowing of the bowel and a longer retention time in the stomach and gut.

Outside the gut, your GI system also expresses taste receptors in the pancreas. You are constantly sensing how much sugar is your blood, and how much is coming in via your gut absorption. Your pancreas has beta cells that produce insulin to increase the amount of sugar taken up by your cells; this reduces your blood sugar levels.

There are multiple mechanisms by which your pancreas knows to make or release more insulin. Chewing, blood glucose levels, stress levels, exercise, and other signals control the balance between hormone signals that reduce (insulin) or increase (glucagon) blood glucose levels. Now these mechanisms must include sweet receptors on the beta cells.

A 2009 paper showed that functional sweet taste receptors were located on the beta cells in mouse pancreas, they have also been found now in humans. Activation of these receptors by sugars or artificial sweeteners stimulate the beta cells to release insulin and lower blood sugar levels.  A more recent study indicates that fructose is also sensed by sweet receptors on beta cells and can amplify insulin signals triggered by binding glucose. This is just more evidence that postprandial (after a meal) nutrient sensing in the pancreas is mediated, at least in part, through taste receptors.

The hypothalamus works in several systems, including

appetite. Interestingly, different parts of the hypothalamus

are in charge of satiety (being full) and the want of feeding.

Water is a whole other matter. All together, the different

nuclei manage the basic control systems of the body, food

water, temperature, blood pressure, etc.

There are even taste receptors for sugars in your brain. The hypothalamus is a part of your brain – an important part - O.K. so all the parts are important. But it seems that blood glucose sensing is particularly acute in the hypothalamus. This is a little harder than it would seem at first thought. You have to sense the glucose levels without being thrown off by sensing the levels of glucose being metabolized in the cell itself. Since cells manage their internal glucose levels, any monitoring system based on this would always report the same result.

But the hypothalamus expresses sweet receptors on the outside of its neurons. Even more, the numbers of receptors is influenced by the nutrient state of the animal. More glucose sensed in other parts of the body (like the taste receptors of the gut), will result in reduced expression in the hypothalamus. This relates to the function of the hypothalamus in appetite as well. More receptor activity relative to the number of receptors, the more signals will be sent out that you are full.

There are more even brain areas that express taste receptors. A 2012 study shows that the rat brainstem has bitter receptors to sample the extracellular fluids for bitter compounds. This may be to try and act as a late protector of the brain against toxins. We have talked before about how the blood brain barrier is designed to protect the brain from toxins better than the blood vessels of the rest of the body.

Taste receptors in the brain (brainstem, hypothalamus, etc)

are attached to neurons, not epithelial cells. It’s the brain, for

gosh sakes, there’s nothing but neurons. This makes the system

more like smell than taste. No taste cells; the signal is directly

transduced to an action potential.

Perhaps sensing bitter compounds in the brain fluid results in a further clamping down on what molecules can get into the brain by manipulating the BBB. The 2012 paper only speculated that the receptors might have other, non-gustatory functions. We have seen above how taste receptors help sense nutrient levels, so it is plausible that bitter receptors in the brain could be sampling for toxins, and then induce some protective response. I bet that's being studied as we speak.

Lastly, recent evidence may show that monitoring taste receptor expression in different tissues may be moot.  It may be that every cell in your body has taste receptors! It may be that the T1R1+T1R3 amino acid taste receptor is in/on every cell sensing whether it has enough free amino acids available.

Amino acid availability is crucial for cellular function. Your cells are producing new proteins all the time, to replace old proteins and to make different proteins that would respond to changes in cell condition and environment. Without a constant source of amino acid building blocks, each cell has to seek out an amino acid supplier. Autophagy (auto = self, phagy = eat) is the answer in most cases.

In times of low amino acid stores, a 2012 study indicates that decreased signaling through the umami taste receptors on your cells will trigger a cascade of responses and the cells start to digest themselves (autophagy). They will break down organelles and proteins so that the amino acids can be recycled for proteins of immediate need. As you can guess, this isn’t the best way to run a business, robbing Peter to pay Paul, so autophagy beyond the normal (getting rid of unneeded or old structures) will have consequences. Muscle wasting in starved individuals is often a result of autophagy.

Every cell has to have a source of free amino acids. There is a

balance that must be maintained. On the bottom right, “intake”

represents the eating of protein. If that doesn’t occur, then

amino acids must be made from building blocks (bottom left).

If there is intake, then new proteins can be made (synthesis).

But if there is no intake, and little de novo synthesis, then

proteolysis (a form of autophagy) will result in free amino

acids for protein synthesis.

A 2005 paper hypothesized (now proven) that all these extraoral taste receptors on solitary chemosensory cells form a diffuse chemosensory system. The taste buds are just the most visible part of a much larger, more complex system of taste. The big picture – organisms taste themselves to monitor their nutrition and health. This isn’t really an exception, just a huge misconception.

So nature evolved extraoral taste receptors for mammals. Why didn’t it take the next step and get rid of oral taste buds? Come back in a million years and maybe we’ll be tasting with our elbows. Sounds ridiculous, doesn’t it. Well, not so fast. Next week we will see that some organisms taste things with some very peculiar body parts.

Sundaresan S, Shahid R, Riehl TE, Chandra R, Nassir F, Stenson WF, Liddle RA, & Abumrad NA (2013). CD36-dependent signaling mediates fatty acid-induced gut release of secretin and cholecystokinin. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 27 (3), 1191-202 PMID: 23233532

Kyriazis GA, Soundarapandian MM, & Tyrberg B (2012). Sweet taste receptor signaling in beta cells mediates fructose-induced potentiation of glucose-stimulated insulin secretion. Proceedings of the National Academy of Sciences of the United States of America, 109 (8) PMID: 22315413

Wauson EM, Zaganjor E, Lee AY, Guerra ML, Ghosh AB, Bookout AL, Chambers CP, Jivan A, McGlynn K, Hutchison MR, Deberardinis RJ, Cobb MH. (2012). The G protein-coupled taste receptor T1R1/T1R3 regulates mTORC1 and autophagy. Mol Cell., 47 (6), 851-862 DOI: 10.1016/j.molcel.2012.08.001

Dehkordi O, Rose JE, Fatemi M, Allard JS, Balan KV, Young JK, Fatima S, Millis RM, & Jayam-Trouth A (2012). Neuronal expression of bitter taste receptors and downstream signaling molecules in the rat brainstem. Brain research, 1475, 1-10 PMID: 22836012

For more information, see:

Extra-oral taste perception – Most of this information is recent enough that scientific journal articles are the only source of information. Follow the links in the post and those below.

http://www.sciencedirect.com/science/article/pii/S1084952112001462

http://www.sciencedaily.com/releases/2007/08/070820175426.htm

http://www.adelaide.edu.au/news/news64082.html

http://consumer.healthday.com/diabetes-information-10/diet-diabetes-news-178/pancreas-may-taste-fructose-hinting-at-links-to-diabetes-661517.html

http://www.physoc.org/proceedings/abstract/Proc%20Physiol%20Soc%2016PC35

http://www.sciencedirect.com/science/article/pii/S0006291X11001999

Cats Don’t Taste Sweet, But Dogs Taste Salty

Biology concepts – gustatory sense, taste receptors, supertasters

We have discussed recently the reasons organisms taste their food are related to nutritional needs (sweet, umami, salt, fat) and protection from toxins (sour, bitter). Sweet is the exceptional case here because it's the only taste that works across a great range of concentrations. You can sense low levels of sugar, and it just gets sweeter as more sugar is added. For sour, too much is not a great thing – think sour patch kids. And bitter? India pale ales have way too much hops for me.

The idea that sugar is sweet across all concentrations is

challenged anecdotally by Glucola. This is a drink with 50

grams of glucose. It is used to test for diabetes, especially

gestational diabetes. Many people claim it is too sweet,

nectar of the devil they call it. My wife, on the other

hand, asks for more.

This is an amazing preventative measure in organisms – remember that Paracelsus said that only the dose makes the poison – too much of a good thing can be bad – too much protein leads to hyperaminoacidemia and hyperammonemia (too much amino acid and ammonia in blood). Too much salt can throw ionic balance out of whack, and very bitter tastes suggest a toxin. But too much sweet, no way! Evolution decided there is no such thing as too much sugar – the body wants as much energy (carbohydrate) as it can get.

If this is the case, then why can’t cats taste sweet things? It has been known for a while (2005) that all cat species lack a functional Tas1R2 protein, one part of the sweet receptor (other part is Tas1R3). Cats happen to be obligate carnivores – they only eat meat – so they don’t need to crave carbohydrates – they get enough from metabolizing the compounds in the meat.

Now, a 2012 study has expanded the results to other obligate carnivores. Jiang and his group tested many other species for nonfunctional Tas1R2 protein. Included in the list of animals that can’t taste sweet are the asian short-clawed otter, the spotted hyena, seal lions, dolphins, the fossa, and harbour seals.

Other animals, like dogs, giant pandas, termite-eating hyenas (aardwoles), Canadian otters, and raccoons were found to still have functional Tas1R2 proteins, probably because these animals sometimes eat things other than meat.

On the left is the spotted hyena, also known as the laughing hyena.

It is the largest of the hyenas and is an obligate meat eater. The

right picture is of an aardwolf, another species of hyena. Of the

four extant species of hyenas, the aardwolf is the only

insectivore; the aardwolf diverged from the other common

ancestors about 15 million years ago. It has an amazing

digestive system, being one of the few animals that can stand

the terpene compounds held inside soldier termites. The

aardwolf has a sweet sense, but the spotted hyena doesn’t; this

divergence occurred within the last 10 million years or so.

It isn’t just one change that makes Tas1R2 non-functional, the different animals had different changes, so they must have had a common, sweet-tasting ancestor. Some mutations were probably recent; notice that spotted hyenas can’t taste sweet, but termite eating hyenas can. Canadian otters have functional sweet receptors, but asian otters do not.

The 2012 study of Jiang, and another 2012 study indicate that many seal and sea lion species are double losers – they have lost the use of the Tas1R1 protein as well. To taste umami, the receptor is Tas1R1 + Tas1R3. Yet another 2012 study indicated that 31 different species of bat (fruit, insect, and blood feeding) have lost sweet perception), and vampire bats have lost both sweet and umami (non-functional Tas1R1 and Tas1R2 proteins). Apparently, 2012 was a big year for studying taste loss in animals.

But the kings of poor taste may be the bottlenose dolphins. They have non-functional Tas1R1 and Tas1R2, so no sweet or umami for them, but they have also lost about half of the genes for functional bitter receptors. Why? They swallow their food whole – so taste isn’t a big priority for them.

So cats have no sweet perception, but dogs still have it. But dogs are exceptional in another way. They have a reduced ability to taste salt. Dogs seem to have additional receptors for meat contain chemicals, so they really crave meat. But meat is full of salt, so they don’t have to crave it. It gets weirder though.

We said above that too much of something can be bad, and if dogs eat too much meat, they get too much salt. This can throw all ionic mechanisms into chaos, which includes about every function of every cell. Dogs need to balance their salt intake with their water intake – more salt, then more water to flush it out.

Dogs have water receptors on the tip of their tongue.

There increased sensitivity makes them crave water

after eating salt. But lapping doesn’t occur on the top of

their tongue. The pictures show that they actually scoop

water with the back of their tongue, sort of like how the

elephant uses their trunk. They lap it up, they

don’t lick it up.

To do this, dogs and other carnivores have taste receptors for water. We said last week that humans have receptors for water, mostly for the swallowing reflex, but in the cases of dogs and cats, they are hooked up to taste perception. Here’s the amazing part. Dogs may not perceive salt very well, but taking in salt makes their water receptors much more sensitive. This means water will be tastier to them after having eaten meat. This mechanism triggers dogs to drink more water after eating meat so that salt concentrations don’t get too high!

So now we know that taste perception varies across species. How about within a species - do all people taste things similarly? No way, just ask a supertaster.

It was recognized in the 1930’s that some people react to bitter tastes more strongly than other people. A chemical called phenylthiocarbamide (PTC) accidently got loose in a lab, and only some lab members tasted the powder in the air. Now we use a similar chemical called propylthiouracil (PROP, it's safer than PTC) to test if people have a strong bitter taste sense.

About 25% of the population reacts strongly to PROP, these are the supertasters (coined by Dr. Linda Bartoshuk in 1991). Another 15% of people don’t taste it at all. These are the non-tasters. But many people lie somewhere in between – medium tasters.

However, as Dr. Bartoshuk continued researching, it became apparent that there was more going on. Here is where genetics enters the picture. The bitter receptor (Tas2R38, one of 25 or so bitter recptors) for PROP or PTC comes as several different alleles; one which reacts strongly (T), one that reacts weakly (t), and five that are in between and much more rare.

There is basic mendelian dominance here. If you inherited 2 T alleles, you were considered a supertaster. Two t alleles made you a non-taster, and a Tt genotype landed you in the middle. But there was too much variation. Some people with Tt reacted strongly, while others with tt reacted strongly to other tastes (sweet or sour or even umami).

The cartoon on the left shows how The Tas2R38 bitter receptor

alleles can be inherited. If you are TT, then you taste the bitter

chemical PROP very strongly. If you inherit two t alleles, you won’t

taste PROP at all. The majority of us are Tt, we taste it PROP but it

doesn’t gag us. The right cartoon depicts a generic sweet or umami

receptor. They are heterodimer, made up of two different proteins.

Tas1R1 + Tas1R3 = umami perception; Tas1R2 + Tas1R3 = sweet

perception. The bottom part shows that the dimer fits in the membrane

with each protein having seven transmembrane domains

(the grey rectangles).

More must be at work. Dr. Bartoshuk (2013) has been part of research that has now shown that Tas1R1 (part of umami receptor) also comes in different forms, and demonstrates different intensities of reaction. There is also a paper that suggests that because people with sensitive bitter receptors also react strongly to other tastes, there must be a central pathway for taste perception in the brain that is turned up in supertasters.

Because some people react strongly to more than just PROP, scientists changed the definition of supertaster to those that had both increased sensitivity to PROP/PTC and increased sensitivity to other tastes or food qualities. So you have to define now how your supertaster - pST is a supertaster for PROP alone, while gST is for increased sensitivity to several tastes.

This still can’t account for all the variations in taste intensity seen in different people. Dr. Bartoshuk also discovered that people can have different numbers of taste buds. Taste buds house the taste cells that have the taste receptors; more buds means more receptors means more intense taste.

You can easily test if you have a sensitivity to PROP using small pieces of paper soaked in PROP, but you can also see if you have an above average number of taste buds. Take some blue food dye and a ring reinforcer (those little circles you put on papers so the three ring binder won’t tear through the hole punch hole). Put a drop of dye on your tongue and rinse. The darker blue areas are the filliform papillae; they don’t have taste buds.

The classroom is a great place to count fungiform papillae. The close

up on the right shows that the fungiform papillae take up less stain;

they are the roundish bump, not the dark blue areas. Remember, you

are counting papillae, not taste buds – taste buds are housed at and

beneath the surface of the papillae. Each fungiform papillae may

have many taste buds (1-20) with those on the tip of your tongue

having more buds. Each bud has 50-150 taste cells, and each cell

has hundreds of receptors.

The lighter staining, round areas are the fungiform papillae; this is where the taste buds are located. Put the ring reinforcer on your tongue and count the number of fungiform papillae in the open circle. If you count more than 30, you're probably a supertaster.

The number of fungiform papillae is genetically controlled, as is the expression of different receptor alleles, but the mechanism hasn't been worked out yet for taste bud number. The take home message – both the number of receptors and the alleles of the receptors determine if you are a supertaster or not.

On the other end are the non-tasters. If you count fewer than 10 fungiform papillae in the circle on your tongue, you are most likely a non-taster. On average, humans have about 10,000 taste buds. This is many more than dogs (avg. 1700) or cats (avg. 470). Supertasters may have more than 25,000, while non-tasters may have fewer than 5,000. I have no idea how many taste buds a supertasting dog has.

Non-tasters are said to be taste blind, either generally (ageusia, from Latin a = without and geusia = taste), or just to specific tastants (specific ageusia), like PROP for example. But don’t feel bad for the non-tasters; this doesn’t condemn them to tasting nothing. It just takes more for them to get their craving satisfied.

Guess which cartoon character is more likely to depict a

supertaster. The one on the left – it looks like his food is

super tasty. But really, supertasters – on average – have a

harder time finding foods that don’t overpower their taste

buds. Non-tasters are much more likely to find foods that

are not too salty, too sweet, too bitter, too sour, or too savory.

On the other hand, supertasting isn’t always super. Bitter things may be too bitter to enjoy. In general, supertasters survive better in new environments because they are less likely to eat something toxic. But non-tasters are safer in known environments, because they can find more foods that they can enjoy enough to eat. But always remember, this is a complex system that can be overcome by learning. Some people consider some things too sweet, just as supertasters can learn to enjoy very bitter foods.

One last tidbit – for some unknown reason, the myth that the tongue has specific areas for certain tastes is still being propagated. This just isn’t so. There are places where certain receptors may be more or less numerous, but you can sense all tastes on all parts of your tongue. I hope that settles that.

But even this is an incomplete picture of taste. Next week we will discover that you don’t taste with just your tongue. Heck, an insect tastes things, and it doesn’t even have a tongue!



Rawal S, Hayes JE, Wallace MR, Bartoshuk LM, & Duffy VB (2013). Do polymorphisms in the TAS1R1 gene contribute to broader differences in human taste intensity? Chemical senses, 38 (8), 719-28 PMID: 24000232
 
Zhao H, Xu D, Zhang S, & Zhang J (2012). Genomic and genetic evidence for the loss of umami taste in bats. Genome biology and evolution, 4 (1), 73-9 PMID: 22117084
 
Sato JJ, & Wolsan M (2012). Loss or major reduction of umami taste sensation in pinnipeds. Die Naturwissenschaften, 99 (8), 655-9 PMID: 22777285
 
Jiang P, Josue J, Li X, Glaser D, Li W, Brand JG, Margolskee RF, Reed DR, & Beauchamp GK (2012). Major taste loss in carnivorous mammals. Proceedings of the National Academy of Sciences of the United States of America, 109 (13), 4956-61 PMID: 22411809


For more information or classroom activities, see:

Supertasters –

http://www.pbs.org/wgbh/nova/education/activities/0404_01_nsn.html

http://www.scoop.it/t/taste-and-smell

http://sciencenetlinks.com/lessons/a-taste-of-exploratopia/

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=3&ved=0CDsQFjAC&url=http%3A%2F%2Fwww.ifr.ac.uk%2Finfo%2Fsociety%2FTasteandFlavour%2FForTeachers.pdf&ei=FoLZUvL2HqPSyAG8pIDYBA&usg=AFQjCNGU7Rg66soR1GBfyu9G0e5lnlg3LA&sig2=Co1NmKEOchWN06A9G83hqQ&bvm=bv.59568121,d.aWc

https://www.google.com/#q=supertaster+classroom+activity

http://www.bbc.co.uk/science/0/22941835

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=10&ved=0CHIQFjAJ&url=http%3A%2F%2Ffacstaff.gpc.edu%2F~ddonald%2Fbiolab%2FSupertasters.pdf&ei=FoLZUvL2HqPSyAG8pIDYBA&usg=AFQjCNG9tGypJR2RlQxERYA6v2wuJzmOxg&sig2=FzHnZy1mDagmq6WCXrTsRA&bvm=bv.59568121,d.aWc

http://www.abc.net.au/catalyst/stories/3308031.htm

http://www.scientificamerican.com/article.cfm?id=super-tasting-science-find-out-if-youre-a-supertaster

http://science.howstuffworks.com/life/human-biology/taste4.htm

http://online.wsj.com/news/articles/SB10001424127887324392804578362833147151480

http://www.bbc.co.uk/science/humanbody/body/articles/senses/supertaster.shtml

http://www.livescience.com/17190-supertaster-nontaster-tongue-evolution.html

http://www.pbslearningmedia.org/resource/nvsn6.sci.bio.taster/what-is-a-supertaster/

http://www.npr.org/templates/story/story.php?storyId=127914467

http://www.the-scientist.com/?articles.list/tagNo/1290/tags/supertaster/