Bitter taste

A broad spectrum of structurally diverse compounds has a bitter taste, including caffeine, theobromine (the principal alkaloid in cocoa and chocolate), quinine tin tonic

-CH2

6-n-Propy!-2-friiouracil (PROP) Quinine

-CH2

6-n-Propy!-2-friiouracil (PROP) Quinine

Salicin

Salicin

OH O

Naringin (naringenin 7-ji-glucoside) Nicotine

Helicin

OH O

Naringin (naringenin 7-ji-glucoside) Nicotine

Helicin

Theobromine

Arbutin

Theobromine

Caffeine

Arbutin

Caffeine water), nicotine, L-amino acids (with the exception ofL-glutamatc), urea, magnesium and cesium salts, phenols and polyphenols, tlavonoids (naringjn in grapefruit, methyl-naringenin in hops), catechins (in lea), ami local anesthetics. The bitter-tasting compound 6-n-propyI-2-thiouracil (PROP) is commonly used in taste tests (Drewnowski et a!.. 200)). Use oFphcnylthiocarbamide(PTC) for this purpose in humans has been largely discontinued because of its suspected carcinogenicity.

A large family of taste receptors, comprising more than 40 distinct molecular species, senses bitter tastes (Adler et at.. 2000: Matsunami et a/,, 2000). The receptors activate an intracellular signaling cascade \ ia alpha-guslducin. analogous to receptors responding to sweet-tasting compounds. One of these receptors, TRB7 {Matsunami et at., 2000). responds to the test substance PROP (Bartoshuk et at., 19941. Another one. T2R9. senses cycloheximide. While individual taste cells express several different receptors (Adler et at.. 2000; Matsunami et «/„ 2000). humans can still discriminate between several hitter-tasting compounds. It has been suggested that individual bitter-tasting substances preferentially activate distinct subpopulatiOns of taste cells and thereby generate a compound-specific pattern of neuronal signals (Caicedo and Roper. 2001).

Additional mechanisms for bitter taste sensing have been described but arc less well characterized. Thus, the bitter-tasting compound denatonium appears to inhibit outward potassium flow, and possibly induce signaling through the release of intracellular calcium stores (Yan et a/., 2001).

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