Sweetness
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Sweetness is a basic taste most commonly perceived when eating foods rich in sugars. Sweet tastes are generally regarded as pleasurable. In addition to sugars like sucrose, many other chemical compounds are sweet, including aldehydes, ketones, and sugar alcohols. Some are sweet at very low concentrations, allowing their use as non-caloric sugar substitutes. Such non-sugar sweeteners include saccharin, aspartame, sucralose and stevia. Other compounds, such as miraculin, may alter perception of sweetness itself.
The perceived intensity of sugars and high-potency sweeteners, such as aspartame and neohesperidin dihydrochalcone, are heritable, with gene effect accounting for approximately 30% of the variation.[1]
The chemosensory basis for detecting sweetness, which varies between both individuals and species, has only begun to be understood since the late 20th century. One theoretical model of sweetness is the multipoint attachment theory, which involves multiple binding sites between a sweetness receptor and a sweet substance.
Studies indicate that responsiveness to sugars and sweetness has very ancient evolutionary beginnings, being manifest as
Examples of sweet substances
A great diversity of chemical compounds, such as aldehydes and ketones, are sweet. Among common biological substances, all of the simple carbohydrates are sweet to at least some degree. Sucrose (table sugar) is the prototypical example of a sweet substance. Sucrose in solution has a sweetness perception rating of 1, and other substances are rated relative to this.[13] For example, another sugar, fructose, is somewhat sweeter, being rated at 1.7 times the sweetness of sucrose.[13] Some of the amino acids are mildly sweet: alanine, glycine, and serine are the sweetest. Some other amino acids are perceived as both sweet and bitter.
The sweetness of 5% solution of glycine in water compares to a solution of 5.6% glucose or 2.6% fructose.[14]
A number of plant species produce
Name | Type of compound | Sweetness |
---|---|---|
Lactose | Disaccharide | 0.16 |
Maltose | Disaccharide | 0.33 – 0.45 |
Trehalose (α,α-trehalose) | Disaccharide | max. 0,45[21] |
Isomaltulose | Disaccharide | 40 - 50[22] |
Sorbitol | Polyalcohol |
0.6 |
Galactose | Monosaccharide | 0.65 |
Glucose | Monosaccharide | 0.74 – 0.8 |
Glycine | Amino acid | 0.6 – 0.86 |
Sucrose | Disaccharide | 1.00 (reference) |
Xylitol | sugar alcohol | 1,02[23] |
Fructose | Monosaccharide | 1.17 – 1.75 |
Sodium cyclamate | Sulfonate | 26 |
Steviol glycoside | Glycoside | 40 – 300 |
Aspartame | methyl ester |
180 – 250 |
Acesulfame potassium | Oxathiazinone dioxide | 200 |
Sodium saccharin | Sulfonyl |
300 – 675 |
Sucralose | Modified disaccharide | 600 |
Thaumatin | Protein | 2000 |
Neotame | Aspartame analog | 8000 |
Sucrooctate | Guanidine | 162,000 (estimated) |
Bernardame | Guanidine | 188,000 (estimated) |
Sucrononic acid | Guanidine | 200,000 (estimated) |
Carrelame | Guanidine | 200,000 (estimated) |
Lugduname | Guanidine | 230,000 (estimated) |
Some variation in values is not uncommon between various studies. Such variations may arise from a range of methodological variables, from sampling to analysis and interpretation. Indeed, the taste index of 1, assigned to reference substances such as sucrose (for sweetness), hydrochloric acid (for sourness), quinine (for bitterness), and sodium chloride (for saltiness), is itself arbitrary for practical purposes.[18] Some values, such as those for maltose and glucose, vary little. Others, such as aspartame and sodium saccharin, have much larger variation.
Even some inorganic compounds are sweet, including beryllium chloride and lead(II) acetate. The latter may have contributed to lead poisoning among the ancient Roman aristocracy: the Roman delicacy sapa was prepared by boiling soured wine (containing acetic acid) in lead pots.[24]
Hundreds of synthetic organic compounds are known to be sweet, but only a few of these are legally permitted[where?] as food additives. For example, chloroform, nitrobenzene, and ethylene glycol are sweet, but also toxic. Saccharin, cyclamate, aspartame, acesulfame potassium, sucralose, alitame, and neotame are commonly used.[citation needed]
Sweetness modifiers
A few substances alter the way sweet taste is perceived. One class of these inhibits the perception of sweet tastes, whether from sugars or from highly potent sweeteners. Commercially, the most important of these is
Two natural products have been documented to have similar sweetness-inhibiting properties:
On the other hand, two plant proteins,
The sweetness receptor
Despite the wide variety of chemical substances known to be sweet, and knowledge that the ability to perceive sweet taste must reside in taste buds on the tongue, the biomolecular mechanism of sweet taste was sufficiently elusive that as recently as the 1990s, there was some doubt whether any single "sweetness receptor" actually exists.
The breakthrough for the present understanding of sweetness occurred in 2001, when experiments with
Human studies have shown that sweet taste receptors are not only found in the tongue, but also in the lining of the gastrointestinal tract as well as the nasal epithelium, pancreatic islet cells, sperm and testes.[30] It is proposed that the presence of sweet taste receptors in the GI tract controls the feeling of hunger and satiety.
Another research has shown that the threshold of sweet taste perception is in direct correlation with the time of day. This is believed to be the consequence of oscillating leptin levels in blood that may impact the overall sweetness of food. Scientists hypothesize that this is an evolutionary relict of diurnal animals like humans.[31]
Sweetness perception may differ between species significantly. For example, even amongst the primates sweetness is quite variable. New World monkeys do not find aspartame sweet, while Old World monkeys and apes (including most humans) all do.[32] Felids like domestic cats cannot perceive sweetness at all.[33] The ability to taste sweetness often atrophies genetically in species of carnivores who do not eat sweet foods like fruits, including bottlenose dolphins, sea lions, spotted hyenas and fossas.
Sweet receptor pathway
To depolarize the cell, and ultimately generate a response, the body uses different cells in the taste bud that each express a receptor for the perception of sweet, sour, salty, bitter or umami. Downstream of the taste receptor, the taste cells for sweet, bitter and umami share the same intracellular signalling pathway.[34] Incoming sweet molecules bind to their receptors, which causes a conformational change in the molecule. This change activates the G-protein, gustducin, which in turn activates phospholipase C to generate inositol trisphosphate (IP3), this subsequently opens the IP3-receptor and induces calcium release from the endoplasmic reticulum. This increase in intracellular calcium activates the TRPM5 channel and induces cellular depolarization.[35][36] The ATP release channel CALHM1 gets activated by the depolarization and releases ATP neurotransmitter which activates the afferent neurons innervating the taste bud.[37][38]
Cognition
The color of food can affect sweetness perception. Adding more red color to a drink increases its perceived sweetness. In a study darker colored solutions were rated 2–10% higher than lighter ones despite having 1% less sucrose concentration.[39] The effect of color is believed to be due to cognitive expectations.[40] Some odors smell sweet and memory confuses whether sweetness was tasted or smelled.[41]
Historical theories
The development of
In 1919, Oertly and Myers proposed a more elaborate theory based on a then-current theory of color in synthetic dyes. They hypothesized that to be sweet, a compound must contain one each of two classes of structural motif, a glucophore and an auxogluc. Based on those compounds known to be sweet at the time, they proposed a list of six candidate glucophores and nine auxoglucs.
From these beginnings in the early 20th century, the theory of sweetness enjoyed little further academic attention until 1963, when
B-X theory was proposed by
MPA theory
The most elaborate theory of sweetness to date is the multipoint attachment theory (MPA) proposed by Jean-Marie Tinti and Claude Nofre in 1991. This theory involves a total of eight interaction sites between a sweetener and the sweetness receptor, although not all sweeteners interact with all eight sites.[42] This model has successfully directed efforts aimed at finding highly potent sweeteners, including the most potent family of sweeteners known to date, the guanidine sweeteners. The most potent of these, lugduname, is about 225,000 times sweeter than sucrose.
References
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General
- Cohn, Georg (1914). Die Organischen Geschmackstoffe. Berlin: F. Siemenroth.
- Dobbing, John, ed. (1987). Sweetness. (papers presented at a symposium held in Geneva, May 21–23, 1986). London: Springer-Verlag. ISBN 978-0-387-17045-9.
- Kier L (1972). "A molecular theory of sweet taste". Journal of Pharmaceutical Sciences. 61 (9): 1394–1397. PMID 5068944.
- Kitagawa M, Kusakabe Y, Miura H, Ninomiya Y, Hino A (2001). "Molecular genetic identification of a candidate receptor gene for sweet taste". Biochemical and Biophysical Research Communications. 283 (1): 236–242. PMID 11322794.
- Max M, Shanker YG, Huang LQ, Rong M, Liu Z, Campagne F, Weinstein H, Damak S, Margolskee RF (2001). "Tas1r3, encoding a new candidate taste receptor, is allelic to the sweet responsiveness locus Sac". Nature Genetics. 28 (1): 58–63. PMID 11326277.
- Montmayeur JP, Liberles SD, Matsunami H, Buck LB (2001). "A candidate taste receptor gene near a sweet taste locus". Nature Neuroscience. 4 (5): 492–8. S2CID 21010650.
- Nelson G, Hoon MA, Chandrashekar J, Zhang YF, Ryba NJP, Zuker CS (2001). "Mammalian sweet taste receptors". Cell. 106 (3): 381–390. S2CID 11886074.
- Nofre C, Tinti JM (1996). "Sweetness reception in man: the multipoint attachment theory". Food Chemistry. 56 (3): 263–274. .
- Parkes, A.S (January 1963). "Olfactory and Gustatory Discrimination in Man and Animals". PMID 13941509.
- Sainz E, Korley JN, Battey JF, Sullivan SL (2001). "Identification of a novel member of the T1R family of putative taste receptors". Journal of Neurochemistry. 77 (3): 896–903. S2CID 11296598.
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- Schiffman, Susan S.; Lockhead, Elaine; Maes, Frans W (October 1983). "Amiloride reduces the taste intensity of Na+ and Li+ salts and sweeteners". Proc. Natl. Acad. Sci. U.S.A. 80 (19): 6136–640. PMID 6577473.
- Schiffman, S.S.; Diaz, C; Beeker, T.G (March 1986). "Caffeine Intensifies Taste of Certain Sweeteners: Role of Adenosine Receptor". Pharmacology Biochemistry and Behavior. 24 (3): 429–432. S2CID 20419613.
- Susan S. Schiffman; Elizabeth A. Sattely-Miller (2000). "Synergism among Ternary Mixtures of Fourteen Sweeteners". Chemical Senses. 25 (2): 131–140. PMID 10781019.
- Shallenberger RS (1963). "Hydrogen bonding and the varying sweetness of the sugars". Journal of Food Science. 28 (5): 584–9. .
- Tinti, Jean-Marie; Nofre, Claude (1991). "Why does a sweetener taste sweet? A new model". In Walters, D.E.; Orthoefer, F.T; DuBois, G.E. (eds.). Sweeteners: Discovery, Molecular Design, and Chemoreception. ACS Symposium Series. Vol. 450. Washington DC: American Chemical Society. pp. 209–213.
Further reading
- Castro DC, Berridge KC (2014). "Opioid hedonic hotspot in nucleus accumbens shell: mu, delta, and kappa maps for enhancement of sweetness "liking" and "wanting"". J. Neurosci. 34 (12): 4239–50. PMID 24647944.
- Peciña S, Berridge KC (2005). "Hedonic hot spot in nucleus accumbens shell: where do mu-opioids cause increased hedonic impact of sweetness?". J. Neurosci. 25 (50): 11777–86. PMID 16354936.