The sensations of bitter and sour keep us from eating potentially toxic substances and strong acids, while the preferred qualities of sweet, umami (the “savoury” taste of glutamate), and salty drive intake of carbohydrates, amino acids, and sodium, respectively.
Our taste sensations are mediated by taste buds, described as small clusters of specialised epithelial cells found on the tongue, soft palate, and larynx. In the last 20 years or so additional special receptors called G-Protein coupled receptor cascades (GPCRs) and related ion channel are intimately involved with the interpretation of tastes and related signalling.
But it is not just the taste buds that are involved with these receptors; they are also in the stomach, intestines and lungs. Yet as you will have discovered it is only those in the mouth that relay taste, the others it appears have different but important functions.
Tasty Sensations
As we all know, even if we cannot remember why, our taste buds have 5 distinct qualities:
- Salty,
- Sour,
- Bitter,
- Sweet, and
- Umami.
Salty and sour sensory perceptions rely on ion channels, which are expressed in a variety of tissues, such as kidney, as well as in taste buds. Bitter, sweet, and umami qualities rely predominantly on a couple of specific GPCRs, found in the mouth, lungs and gut. Despite the difference in the qualities detected by the two families of taste receptors, both utilise similar, if not identical, downstream signalling effectors, including the taste receptor-associated G protein α-gustducin.
Your Guts Can Taste!
Back in 1996 Researchers described this particular G Protein as being found in the brush border of the stomach and the intestines.[1]In 1996, researchers at the University of Würzburg reported that α-gustducin is expressed by brush cells of the stomach and intestine.This suggested that brush cells detect nutrients in the gut. In the last 15 years, researchers have uncovered more and more taste cascade elements throughout the digestive tract, and even in the airways, suggesting a widespread distribution of complete taste transduction cascades.
Yet they are not taste delivering receptors, rather they contribute to physiological effects in the body, such as insulin promotion, which in part at least is activated by the binding of glucose to sweet-taste receptors on cells of the intestine and subsequent activation of the signaling cascade.[2] In the same way these receptors, will in the case of inhaled drink make us cough or choke. In fact, the receptors mediating taste transduction appear to have evolved early in our genetic development, and to have since been widely adopted as a chemodetection system in a variety of organ systems.
The usefulness of these chemoreceptors in the gut are being linked to defensive mechanisms that include the rapid excretion of toxins via the induction of fluid ingress. Thus, activation of taste signalling in the intestines indirectly results in increased elimination of absorbed toxins from gut epithelium before the toxins can enter circulation.
Lower in the gut, activation of taste receptors similarly appears to combat toxins, though via a different mechanism. When some bitter-tasting ligands bind to epithelial cells in the colon, they induce the secretion of anions, which leads to fluid secretion into the intestine.[3] This induced efflux of fluids is likely to flush out any noxious irritant from the colon, resulting in diarrhoea.
“Taste” in the airways
Taste receptors found in the nasal tissues when activated produce a sensation of irritation and pain. In addition, activation of these fibres evokes protective airway reflexes such as apnoea (to prevent further inhalation) and sneezing (to remove the irritant). Thus, inhalation of a toxin that activates taste receptors will be irritating and will provoke changes in respiration, but will not, of course, produce the sensation of a bitter taste.[4]
More recently, it has been confirmed that some bacterial metabolites and signal molecules can activate the nasal taste receptors and the closely associated trigeminal nerve. Upon activation, the trigeminal nerve fibres not only transmit the information towards the brain, but also release peptide modulators (such as substance P and calcitonin gene-related peptide) into the local tissue, including around nearby blood vessels. These modulators bind to receptors on mast cells and blood vessels, causing a local, neurally mediated inflammation of the airway lining. In this way, nasal taste receptors not only act as sentinels warning against inhalation of irritants, but also serve as guardians capable of activating the innate immune system to respond to the presence of potentially damaging toxins or pathogens.
Remaining taste mysteries
It is evident that taste receptors and their associated downstream signaling components are widely dispersed in diverse organ systems, and in many cases serve to help with digestion or to protect cells from potential toxins. But taste receptors have also been identified in other organs and tissues, such as the bile ducts, where their functions are still unclear. The composition of the fluid in the bile ducts is dictated by secretions of the pancreas, liver, and gall bladder. Why should it be necessary to diligently monitor the composition of biliary fluids as they move from gall bladder to intestine?
References
[1] D. Höfer et al., “Taste receptor-like cells in the rat gut identified by expression of alpha-gustducin,” PNAS, 93:6631-34, 1996. View Abstract
[2] H.J. Jang et al., “Gut-expressed gustducin and taste receptors regulate secretion of glucagon-like peptide-1,” PNAS, 104:15069-74, 2007. View Abstract
[3] I. Kaji et al. “Secretory effects of a luminal bitter tastant and expressions of bitter taste receptors, T2Rs, in the human and rat large intestine,” Am J Physiol Gastrointest Liver Physiol, 296:G971-81, 2009. View Abstract
[4] M. Tizzano et al., “Nasal chemosensory cells use bitter taste signaling to detect irritants and bacterial signals,” PNAS, 107:3210-15, 2010. View Abstract
