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Main article: Taste perception

Bitterness is the most sensitive of the tastes, and is perceived by many to be unpleasant, sharp, or disagreeable. Common bitter foods and beverages include coffee, unsweetened cocoa, South American "mate", marmalade, bitter melon, beer, bitters, olives, citrus peel, many plants in the Brassicaceae family, dandelion greens and escarole. Quinine is also known for its bitter taste and is found in tonic water. The threshold for stimulation of bitter taste by quinine averages 0.000008 M.[1] The taste thresholds of other bitter substances are rated relative to quinine, which is given an index of 1.[1][2] 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.[1] The most bitter substance known is the synthetic chemical denatonium, which has an index of 1,000.[2] It is used as an aversive agent that is added to toxic substances to prevent accidental ingestion. This was discovered in 1958 during research on lignocaine, a local anesthetic, by Macfarlan Smith of Edinburgh, Scotland</sup>.

Research has shown that TAS2Rs (taste receptors, type 2, also known as T2Rs) such as TAS2R38 coupled to the G protein gustducin are responsible for the human ability to taste bitter substances.[3] 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).[4] Researchers use two synthetic substances, phenylthiocarbamide (PTC) and 6-n-propylthiouracil (PROP) to study the genetics 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.[5] This genetic variation in the ability to taste a substance has been a source of great interest to those who study genetics.

In addition, it is of interest to those who study evolution, as well as various health researchers[1][6] since PTC-tasting is associated with the ability to taste numerous natural bitter compounds, a large number of which are known to be toxic. The ability to detect bitter-tasting, toxic compounds at low thresholds is considered to provide an important protective function.[7][1][6] Plant leaves often contain toxic compounds, yet even amongst leaf-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.[8] Amongst humans, various food processing techniques are used worldwide to detoxify otherwise inedible foods and make them palatable.[9] Recently it is speculated that the selective constraints on the TAS2R family have been weakened due to the relatively high rate of mutation and pseudogenization. [10]

Evolution of bitter taste receptors Edit

Of the five basic tastes, three (sweet, bitter and umami tastes) are mediated by receptors from the G protein-coupled receptor family. Mammalian bitter taste receptors (T2Rs) are encoded by a gene family of only a few dozen members. It is believed that bitter taste receptors evolved as a mechanism to avoid ingesting poisonous and harmful substances. If this is the case, one might expect different species to develop different bitter taste receptors based on dietary and geographical constraints. With the exception of T2R1 (which lies on chromosome 5) all human bitter taste receptor genes can be found clustered on chromosome 7 and chromosome 12. Analyzing the relationships between bitter taste receptor genes show that the genes on the same chromosome are more closely related to each other than genes on different chromosomes. Furthermore, the genes on chromosome 12 have higher sequence similarity than the genes found on chromosome 7. This indicated that these genes evolved via tandem gene duplications and that chromosome 12, as a result of its higher sequence similarity between its genes, went through these tandem duplications more recently than the genes on chromosome 7.



See alsoEdit


  1. 1.0 1.1 1.2 1.3 1.4 Guyton, Arthur C. (1991) Textbook of Medical Physiology. (8th ed). Philadelphia: W.B. Saunders
  2. 2.0 2.1 McLaughlin, S., & Margolskee, R.F. (1994). "The Sense of Taste American Scientist, vol.82, no.6, pp. 538-545
  3. Maehashi, K., M. Matano, H. Wang, L. A. Vo, Y. Yamamoto, and L. Huang (2008). Bitter peptides activate hTAS2Rs, the human bitter receptors. Biochem Biophys Res Commun 365.
  4. Lindemann, Bernd (13 September 2001). Receptors and transduction in taste. Nature 413: 219–225.
  5. Wooding, S., U. K. Kim, M. J. Bamshad, J. Larsen, L. B. Jorde, and D. Drayna (2004). Natural selection and molecular evolution in PTC, a bitter-taste receptor gene. Am J Hum Genet 74.
  6. 6.0 6.1 Logue, A.W. (1986) The Psychology of Eating and Drinking”. New York: W.H. Freeman & Co.
  7. Glendinning, J. I. (1994). Is the bitter rejection response always adaptive?. Physiol Behav 56.
  8. Jones, S., Martin, R., & Pilbeam, D. (1994) The Cambridge Encyclopedia of Human Evolution. Cambridge: Cambridge University Press
  9. Johns, T. (1990). With Bitter Herbs They Shall Eat It: Chemical ecology and the origins of human diet and medicine. Tucson: University of Arizona Press
  10. Wang, X., S. D. Thomas, and J. Zhang (2004). Relaxation of selective constraint and loss of function in the evolution of human bitter taste receptor genes. Hum Mol Genet 13.
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