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).
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.
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.
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.
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.
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.
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.